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PubMed2000

Meningeal cells can communicate with astrocytes by calcium signaling.

Mechanical stimulation of adult human and rat pia-arachnoid cell cultures (loaded with calcium indicator dye) produced an increase in calcium in the stimulated cell. This change then propagated rapidly among neighboring cells, producing a calcium wave with a maximum distance of propagation and velocity resembling calcium waves in astrocytes. The pia-arachnoid waves were blocked by either octanol or apyrase, suggesting that propagation might occur either by gap junction communication or extracellular movement of ATP. Calcium waves in pia-arachnoid cells could invade contiguous astrocytes, and vice versa. Gap junction coupling between pia-arachnoid cells and astrocytes was shown by dye transfer experiments, in conjunction with immunostaining for connexin43. We infer that calcium signals from cells in the cortical parenchyma may be transmitted to the pia-arachnoid and might then serve in the induction of neurovascular changes, including those postulated to be responsible for the pain of migraine headache.

Astrocytes↗
PubMed2004

Distribution of caveolin-1 in bovine lens and redistribution in cultured bovine lens epithelial cells upon confluence.

The distribution of caveolin-1 in the lens and lens epithelial cells was determined to assess possible roles in cholesterol trafficking, cell to cell communication and signal transduction. Bovine lenses and cultured bovine lens epithelial cells (BLEC) were divided into subcellular fractions and the distribution of proteins recognized by three different caveolin-1 antibodies determined. The immunolocalization of caveolin-1 in the lens epithelium and in subconfluent and confluent cultured BLEC was probed by fluorescence microscopy and laser scanning confocal microscopy. EGF induced phosphorylation of caveolin-1 was detected by Western blotting with an anti-phosphotyrosine antibody to immunoprecipitated caveolin-1 from BLEC and human cancer cells. Monomeric caveolin-1 of about 26 kDa was detected in the epithelial cell membrane of cultured BLEC and fresh epithelia and in the plasma membrane fraction of lens cortical fiber cells. Caveolin-1 of cultured BLEC redistributed from the cytoplasm to plasma membrane as the cells proceeded from subconfluent to confluent states. The apparent abundance of caveolin-1 in cortical fiber cell plasma membrane is consistent with possible roles in distribution of lens membrane cholesterol and membrane structure. The presence of caveolin-1 in the plasma membrane of epithelial cells at - but not before - confluency is consistent with a role of caveolin-1 in cell to cell communications. EGF stimulated phosphorylation of caveolin-1 in human A431 cells but not lens cells.

Animals↗
PubMed2024

MONOCYTES AND B CELLS MEDIATE ALTERATIONS IN THE GENETIC ASSOCIATION BETWEEN PLATELETS AND SEPSIS VIA CLEC SIGNALING PATHWAY.

Background: Sepsis is a life-threatening condition characterized by multiple organ dysfunction. Blood cells abnormalities play a significant role in the onset and progression of sepsis; however, the potential causal relationship between platelets and sepsis remains unclear, as does whether immune cells mediate the interaction between platelets and sepsis. This study aims to explore the potential causal relationship between platelets and sepsis and analyze the mediating effect of immune cells. In addition, cell-to-cell communication was analyzed to explore the interaction between blood cells and immune cells. Material and methods: In this study, genome-wide association study data were utilized to examine the association between blood cells and sepsis. Two-sample Mendelian randomization (MR) and reverse MR were performed to investigate the potential causal relationship between blood cells and sepsis, with a specific focus on the relationship between platelets and sepsis. Subsequently, two-step MR was employed to identify the immune cells that mediate the interaction between platelets and sepsis and to assess their potential mediating effects. Cellchat software was used to analyze cell-to-cell communication. Results: The results of two-sample MR indicated that platelets were negatively correlated with sepsis (OR = 0.976, 95% CI 0.959-0.993, P = 0.005), suggesting that platelets have a protective effect against sepsis. Additionally, reverse MR demonstrated that sepsis had no significant effect on platelets (OR = 0.909, 95% CI 0.156-5.296, P = 0.916). The mediating effect analysis revealed that monocytes and B cells were important mediators in the relationship between platelets and sepsis. Notably, the correlation between platelets and sepsis shifted from negative to positive with the involvement of monocytes and B cells. The number and strength of cell-cell interactions were decreased in sepsis. Monocytes and B cells primarily regulate platelets through the CLEC signaling pathway, contributing to the pathogenesis of sepsis. Conclusion: This study confirmed the protective role of platelets in sepsis. Monocytes and B cells mediate changes in the genetic association between platelets and sepsis. Monocytes and B cells primarily interact with platelets via the CLEC pathway, thereby modulating the genetic association between platelets and sepsis. These findings indicate that thrombocytopenia, especially when accompanied by elevated monocytes and B cells, may serve as a potential marker for sepsis.

Humans↗
PubMed1996

Glia-neuron intercommunications and synaptic plasticity.

It is established that astrocytes are the intimate partner of neurons throughout their lifespan. However, astrocytes play different roles at different stages of the lifespan. During neurogenesis and early development, glial cells provide a scaffold for the correct migration of neurons and growth cones. They provide guidance cues and may also be involved in neuronal proliferation. In the adult, astrocytes maintain neuronal homeostasis and synaptic plasticity. This review discusses some of the cell-cell communication signals which are involved in the maintenance of synaptic plasticity. They are divided into: (a) glia-to-glia signaling, which involves non-synaptic communication by coupling of astrocytes. In this cell communication, cytoplasmic exchange of ions and small molecules among cells is accomplished through cell coupling of cells via cell-to-cell contacts, termed gap junctions; (b) neuron-to-glia signaling, which involves synaptic interactions. This cell-cell intercommunication has received considerable attention. Of special interest is the role of astrocytes in glutamic acid compartmentation and in preventing glutamic acid neurotoxicity. A glutamate-induced calcium signaling appears to be involved in this neuron-astrocyte interaction. The intriguing possibility is that neuronally induced astrocyte calcium signals may feed back to influence neuronal excitability or regulate synaptic transmission; (c) signals from astrocytes to neurons: a new concept of neuron-glia intercommunication. As mentioned, calcium appears to be the molecule in this glia-neuron signaling, although glial cell receptor-mediated signals are involved also. Receptor interactions on astrocytes through a cascade of events lead to modification in the extracellular concentration of glutamate. The role of astrocytes in synaptic plasticity is not as well understood during ageing and their role in neuronal cell death during ageing and neurodegeneration can only be speculated. However, astrocytes in the aged brain exhibit various receptors, including glutamate receptors. Thus, astrocytes can be expected to modify the expression of endogenous neurotoxins and thus contribute to synaptic plasticity in ageing. Synaptic plasticity continues to be a homeostatic relationship between neurons and glial cells. The possibility of signaling from astrocytes to neurons has opened new horizons for glial cell function and new challenges of research for gliobiologists.

Animals↗
PubMed2000

Differential effect of subcellular localization of communication impairing gap junction protein connexin43 on tumor cell growth in vivo.

There is a large body of evidence suggesting the connexin gap junction proteins appear to act as tumor suppressors, and their tumor inhibitory effect is usually attributed to their main function of cell coupling through gap junctions. However, some cancer cells (e.g. the rat bladder carcinoma BC31 cell line) are cell-cell communication proficient. Using specific site-directed mutagenesis in the third membrane-spanning (3M) domain of connexin43 (Cx43), we abolished the intrinsic gap junction intercellular communication (GJIC) in BC31 cells either by closing the gap junctional channels or by disruption of the transport of connexin complexes to the lateral membrane. Clones of BC31 cells transfected with a dominant negative Cx43 mutant giving rise to gap junctional channels, permeable only for a small tracer (neurobiotin), displayed accelerated growth rate in vivo, showing the critical role of selective gap junctional permeability in the regulation of cell growth in vivo. The use of other dominant-negative mutants of Cx43 also suggested that the effect of impaired communication on the tumorigenicity of cancer cells depends on the subcellular location of connexin. Inhibition of intrinsic GJIC in BC31 cells by sequestering of Cx protein inside the cytoplasm, due to expression of dominant-negative transport-deficient Cx43 mutants, did not significantly enhance the growth of transfectants in nude mice, but occasionally slightly retarded it. In contrast, augmentation of GJIC in BC31 cells by forced expression of wild-type Cx43, or a communication-silent mutant, fully suppressed tumorigenicity of these cells. Overall, these results show that cell coupling is a strong, but not the sole, mechanism by which Cx suppresses growth of tumorigenic cells in vivo; a GJIC-independent activity of Cx proteins should be considered as another strong tumor-suppressive factor.

Animals↗
PubMed2003

Concentrations of ouabain that prevent intercellular communication do not affect free calcium levels in cultured fibroblasts.

To better understand inhibition of gap-junction-mediated cell communication among cultured fibroblasts treated with the sodium pump inhibitor ouabain, we tested whether such cells have higher calcium levels than normal. Using the calcium indicator dye fura-2 with fluorescence spectroscopy and digital imaging microscopy, we determined cell calcium levels during exposure of cells to ouabain. The concentration of ouabain was high enough to achieve maximum alterations of steady-state sodium and potassium content and cell communication. We found no consistent change in calcium levels in human fibroblasts as a result of this treatment. In mouse 3T3 fibroblasts, concentrations of ouabain that inhibit cell communication were associated with a significant reduction of cell calcium. It appears, therefore, that the inhibition of communication by ouabain cannot be attributed to elevated cytosolic free calcium in the treated cultures.

Animals↗
PubMed2026

Integrated single-cell and bulk transcriptomic analysis identifies a novel senescent fibroblast subtype associated with poor prognosis in acral melanoma.

BACKGROUND: Acral melanoma (AM) exhibits significant intratumoral heterogeneity, but its tumor microenvironment (TME) and immune regulation remain unclear. This study aims to dissect TME heterogeneity and establish a prognostic model based on key cell subpopulations. METHODS: We collected AM single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA). Unsupervised clustering, CellChat, and Scissor analysis were performed to characterize cellular heterogeneity, cell-cell communication, and prognosis-related cell subpopulations. Kaplan-Meier analysis was used to assess the prognostic value of key genes, which were further validated by multiplex immunohistochemistry (mIHC). RESULTS: In AM, Mel_C2, C7, and C9 with high SEMA6A and KIT expression were strongly linked to poor prognosis. We further identified a senescent fibroblast subpopulation (sCAF_CDKN2A) characterized by high fibroblast senescence signature (FSS) scores. Integrating Scissor analysis of fibroblast subtypes with bulk prognostic data, we identified COL3A1, VCAN, and KIT as prognosis-associated genes upregulated in poor-outcome-related fibroblast subsets. Cell-cell communication analysis revealed that sCAF_CDKN2A engages in an immunosuppressive network, interacting with regulatory T cells (Tregs) via MIF signaling and receiving signals from exhausted CD8+ T cells through PPIA-BSG interactions. Using transcription factor expression patterns from these fibroblast subtypes, we constructed a prognostic model that effectively stratified patients into distinct risk groups with significant differences in overall survival (OS). mIHC confirmed significantly higher protein levels of SEMA6A and COL3A1 in tumor tissues compared to matched normal tissues. CONCLUSIONS: We established a novel prognostic model for AM and identified sCAF_CDKN2A as an immunosuppressive senescent fibroblast subpopulation driving poor prognosis.

Acral melanoma↗
PubMed2003

Lycopene oxidation product enhances gap junctional communication.

Carotenoids as well as their metabolites and oxidation products stimulate gap junctional communication (GJC) between cells, which is thought to be one of the protective mechanisms related to cancer-preventive activities of these compounds. Increased intake of lycopene by consumption of tomatoes or tomato products has been epidemiologically associated with a diminished risk of prostate cancer. Here, we report a stimulatory effect of a lycopene oxidation product on GJC in rat liver epithelial WB-F344 cells. The active compound was obtained by complete in vitro oxidation of lycopene with hydrogen peroxide/osmium tetroxide. For structural analysis high performance liquid chromatography, gas chromatography coupled with mass spectrometry, ultraviolet/visible-, and infrared spectrophotometry were applied. The biologically active oxidation product was identified as 2,7,11-trimethyl-tetradecahexaene-1,14-dial. The present data indicate a potential role of lycopene degradation products in cell signaling enhancing cell-to-cell communication via gap junctions.

Animals↗
PubMed1977

Intercellular communication and tissue growth: IX. Junctional membrane structure of hybrids between communication-competent and communication-incompetent cells.

The structure of the membrane junctions of the hybrid cell system, examined in the companion paper in respect to competence for communication through cell-to-cell membrane channels, is here examined by freeze-fracture electron microscopy. The junctions of the channel-competent parent cell and of the channel-competent hybrid cells present aggregates of intramembranous particles typical of "gap junction"; those of the channel-incompetent parent cell and channel-incompetent segregant hybrid cells do not. Competence for junctional communication and for gap junction formation are genetically related. The junctions of the intermediate hybrid cells with incomplete channel-competence (characterized by cell-to-cell transfer of small inorganic ions but not of fluorescein), present special intramembranous fibrillar structures instead of discrete gap-junctional particles. The possibility that these structures may constitute coupling elements with subnormal permeability is discussed in terms of incomplete dominance of the genetic determinants of gap junction.

Animals↗
PubMed1997

Ligation of CD53/OX44, a tetraspan antigen, induces homotypic adhesion mediated by specific cell-cell interactions.

The CD53 antigen is a member of the tetraspan family of proteins with unknown function. Stimulation of rat IR938F B-cell lymphoma cells with monoclonal antibody MRC OX44 (anti-rat CD53) triggered a homotypic adhesion reaction which reached a maximum effect at 24 hr. This effect occurred at 37 degrees C but not at 4 degrees C. Adhesion was prevented by removal of divalent cations, Ca2+ and Mg2+, with EGTA and EDTA as chelating agents. The adhesion induced by MRC OX44 was inhibited by cycloheximide and actinomycin D, suggesting that de novo protein synthesis was required for this effect. The addition of mAb WT1 against rat LFA-1 (CD11a) antigen had no effect on adhesion, suggesting that the cell-cell interaction is not mediated by the expression of LFA-1 antigen. The intracellular signals required to induce adhesion were inhibited by two tyrosine kinase inhibitors, genistein and piceatannol. Wortmannin, a selective inhibitor of phosphoinositide 3-kinase activity, completely blocked adhesion. Two protein kinase C inhibitors, H7 and bisindolylmaleimide, inhibited the adhesion, suggesting that part of the signal is mediated by PKC. Electron microscopy of aggregated cells showed that the interaction is localized to short membrane regions, where contact areas of higher density in opposing zones from both cells were detected. We postulate that there is a common adhesion mechanism that is modulated by several tetraspan family members and associated proteins. This adhesion structure might represent a novel form of cell communication among lymphoid cells.

Animals↗
PubMed2000

Clustering of connexin 43-enhanced green fluorescent protein gap junction channels and functional coupling in living cells.

Communication-incompetent cell lines were transfected with connexin (Cx) 43 fused with enhanced green fluorescent protein (EGFP) to examine the relation between Cx distribution determined by fluorescence microscopy and electrical coupling measured at single-channel resolution in living cell pairs. Cx43-EGFP channel properties were like those of wild-type Cx43 except for reduced sensitivity to transjunctional voltage. Cx43-EGFP clustered into plaques at locations of cell-cell contact. Coupling was always absent in the absence of plaques and even in the presence of small plaques. Plaques exceeding several hundred channels always conferred coupling, but only a small fraction of channels were functional. These data indicate that clustering may be a requirement for opening of gap junction channels.

Animals↗
PubMed1987

Development of intercellular communication during the epithelial reorganization of a renal cell line (LLC-PK1).

Junctional permeability determinations after microinjection of the fluorescent tracer, Lucifer Yellow CH, show that the cells in confluent monolayers of the renal epithelial cell lines LLC-PK1 and A6 are interconnected by intercellular junctions. This cell-to-cell communication network permits the fluorescent dye to diffuse from the microinjected cell into multiple adjacent neighboring cells. Cell-to-cell diffusion of the fluorescent dye was not observed at pH 6.0. Full recovery occurred, however, when the pH of the extracellular medium was adjusted to 7.4. To provide a sensitive index of the averaged efficacy of junctional communication, we measured the number of cells that survived ouabain treatment in a 50% mixture of wild and ouabain-resistant mutant LLC-PK1 cells. Electron probe microanalysis in uncoupled cells showed that ouabain treatment produced two populations of cells, with totally different intracellular Na+ and K+ content. Under this condition, only 50% of the population survived after 48 h of treatment. When ouabain treatment was initiated 24 h after plating, however, 100% survival was observed, and the cells contained uniform intracellular Na+ and K+ concentration. This finding is consistent with the theory that this protective effect is mediated through the presence of the functional communicating intercellular junctions. When ouabain was applied at different times after plating, full protection is reached by 2 h. The early development of cell-to-cell communication, which precedes the development of the occluding junctions and several transport systems by several hours, is consistent with the involvement of the intercellular junctions in the synchronization of the polarization process.

Cell Communication↗
PubMed2000

Induction of gap junctional intercellular communication, connexin43 expression, and subsequent differentiation in human fetal neuronal cells by stimulation of the cyclic AMP pathway.

Expression of gap junction proteins and cell-cell communication was studied in the human neural-glial cell line, SVG, as a first step in defining whether the SVG cells could be used as a model system to study the role of gap junctions in neuronal precursor cells. SVG cells were found to express connexin43 protein that co-migrated with WB-F344 rat liver connexin43 and that reacted with connexin43-specific antibodies on Western blots. However, fluorescence recovery after photobleaching analysis of 5,6-carboxyfluorescein-loaded cells failed to show significant dye coupling. Agents that stimulate the adenylyl cyclase/cAMP pathway were used to induce gap junctional intercellular communication in the SVG cultures. A 24-48 h treatment of SVG cells with 5 microM forskolin or 5 microM forskolin + 200 microM 3-isobutyl-1-methylxanthine increased the percentage of dye-coupled cells from 5-65%, using the fluorescent recovery after photobleaching method. The increase in dye coupling induced by forskolin or forskolin + 3-isobutyl-1-methylxanthine was inhibited by octanol, which is known to block gap junction-mediated cell communication. Western blot analysis of total protein extracts revealed the appearance of a higher molecular weight connexin43 protein band after treatment of SVG cells with forskolin or forskolin + 3-isobutyl-1-methylxanthine, that was not observed in vehicle-treated controls. Alkaline phosphatase treatment of total protein extracts from forskolin or forskolin + 3-isobutyl-1-methylxanthine-treated cells reduced the higher molecular weight band to approximately 41,000 the same as observed in the control extracts. The alkaline phosphatase treatment demonstrates that the higher molecular weight band was due to a phosphorylation event stimulated by forskolin or the forskolin + 3-isobutyl-1-methylxanthine combination. In addition, treatment of the SVG cells with the forskolin or forskolin + 3-isobutyl-l-methylxanthine stimulated outgrowth of neurite-like processes from the cell body which immunostained positive for the connexin43 protein as well as protein markers for neurons and oligodendrocytes. We hypothesize that the SVG cells may represent a neuronal progenitor cell population that has the ability to differentiate when exposed to the appropriate signals.

1-Methyl-3-isobutylxanthine↗
PubMed1997

Hyperinsulinemia-induced hypoglycemia is enhanced by overexpression of connexin 43.

To assess whether cell to cell communications via connexins (Cx) participate to insulin secretion in vivo, we studied insulinoma cells (INS1) implanted in rats after stable transfection with connexin 43 (Cx43). We found that compared to wild-type and transfected cells, which in vivo express modest levels of Cx43 and junctional communication, cells overexpressing Cx43 communicated extensively, featured decreased growth, and induced a much higher hyperinsulinemia. As a result, rats with insulinomas made of these cells became more severely hypoglycemic than rats implanted with either wild-type, neomycin-transfected cells or cells transfected with a Cx43 antisense complementary DNA. Rats implanted with transfected cells that expressed modest level of Cx43 showed levels of circulating insulin similar to those in rats implanted with wild-type INS1 cells. The data show that overexpression of Cx43 influences the growth and secretion of the implanted insulinoma cells, providing evidence for a contribution of Cx-mediated cell to cell communication in the functioning of insulin-producing cells in vivo.

Animals↗
PubMedDate not supplied

Novel method to examine hepatocyte-specific gene expression in a functional coculture system.

To mimic native tissue function, coculture systems are an extremely useful model. In many cases, differentiated functions can be maintained only through the interactions of various cell types. Therefore, methods for examining the interactions between cocultured cells are necessary. The assessment of cell-to-cell cross-talk at the level of gene expression is one such method to examine interactions between different cell types. However, it is generally difficult to determine the gene expression of specific cell types in coculture without first separating cell populations. To overcome these obstacles, we have established a novel method to determine gene expression levels of a targeted cell population in coculture, using species-specific primers. With this approach, we were able to determine hepatocyte-specific gene expression of Fao cells (a rat hepatocyte cell line) in culture with human umbilical vein endothelial cells (HUVECs). Expression of both albumin and apolipoprotein A-I (apoA-I) increased time dependently for 10 days and maintained significantly higher expression in the coculture system as compared with isolated Fao cells. This indicates that hepatocyte function increased gradually in our coculture system and could be maintained long-term, suggesting that the construction of mature cell-to-cell communication between the two cell lines required a considerable amount of time. The expression of HNF-4 and HNF-1alpha, which are liver-enriched transcription factors, did not differ between the monolayer and cocultured Fao cells, suggesting that expression of HNF-4 and HNF-1alpha was not responsible for the increased expression albumin and apoA-I. Our findings suggest that this novel method for the detection of gene expression of targeted cell populations can be a useful tool in determining the molecular mechanisms that regulate communication between different cell types.

Animals↗
PubMed2003

Use of cocultured cell systems to elucidate chemokine-dependent neuronal/microglial interactions: control of microglial activation.

In order to understand processes involved in central nervous system inflammatory diseases, a critical appreciation of mechanisms involved in the control of immune function in the brain is needed. Microglial cells are watchful eyes for unusual events and detecting the presence of pathogens but are also alert to signals emanating from damaged neurons. Fractalkine (CX3CL1) is a chemokine which is expressed predominantly in the central nervous system, being localized on neurons, while its receptor, CX3CR1, is found on microglial cells. We have developed a strategy to investigate the role of this chemokine in neuronal-microglia interactions. Because fractalkine is expressed both as a soluble and as a membrane-attached protein, we have established various protocols involving different levels of cell-to-cell communication. Three experimental systems were instituted, including (1) a conditioned medium transfer system in which no cell-cell communication or contact is possible, (2) a transwell system that permits cell-contact-independent communication through diffusible soluble factors only, and (3) a coculture system allowing cell-to-cell communication via direct microglial-neuronal contacts. Using these in vitro cocultured systems, we have investigated the role of a soluble and/or cell-associated chemokine, such as fractalkine, in order to obtain insights into the role of glia-neuron interactions in cerebral inflammation.

Animals↗
PubMed1992

Cell interactions influence the pattern of biomineralization in the Ilyanassa obsoleta (Mollusca) embryo.

Ilyanassa obsoleta larvae have two calcium carbonate-containing organs, shell and statocyst, which are derived from five micromere cells (2a, 2c, 2d, 3c, 3d). "Internal shell," an abnormal, internal calcium carbonate mass, was previously observed when cells which normally induce shell and statocyst were removed. This study utilizes multiple-cell deletions to examine how these calcium carbonate-producing precursors control the pattern of biomineralization, whether it is in external shell, statocyst, or internal shell. It was demonstrated that internal shell was solely derived from any of these five cells. However, there was a quantitative difference in the frequency of internal shell production depending upon which cells, as well as how many, are deleted. In general, when external shell or statocyst production was diminished, as the result of removing several of the calcium carbonate-producing cells, internal shell was deposited instead. The presence of internal shell can best be explained as the result of altered interactions between these five cells after one or more have been deleted. Electron diffraction and transmission electron microscopy show that internal shell differs from normal shell in both structure and crystal morphology and it can also be produced by statocyst precursors. Thus, both the deletion and electron microscopy data support the interpretation that the development of internal shell is controlled by shell- and statocyst-producing cells when the cell communication between these cells is disrupted.

Animals↗
PubMed2002

Do bone cells behave like a neuronal network?

Bone cells are organized into an interconnected network, which extends from the osteocytes within bone to the osteoblasts and lining cells on the bone surfaces. There is experimental evidence suggesting that bone tissue exhibits basic properties of short- and long-term memory. An analogy might be made between the bone cell network and neuronal systems. For instance, recent studies suggest that the neurotransmitter glutamate may play a role in cell-to-cell communication among bone cells. Glutamate is a key neurotransmitter involved in learning and memory in reflex loops and the hippocampus. The simplest forms of memory include habituation (desensitization) and sensitization. It is argued that bone cells exhibit habituation to repeated mechanical stimuli and sensitization to mechanical loading by parathyroid hormone (PTH). Acquired long-term memory of a mechanical loading environment may influence the responsiveness of bone tissue to external stimuli. For instance, bone tissue from the skull shows markedly different responses to several stimuli, e.g., mechanical loading, disuse, and PTH, compared with long bones. We speculate that the history of weight bearing imparts long-term cellular memory to the bone cell network that modulates the cellular response to a wide variety of stimuli.

Animals↗