"Acne biofilms," temperature, and microenvironments.
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Acne Vulgaris↗
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Results for “microenvironment”
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Engineering microenvironment for expansion of sensitive anchorage-dependent mammalian cells.
Tissue engineering involves ex vivo seeding of anchorage-dependent mammalian cells onto scaffolds, or transplanting cells in vivo. The cell expansion currently requires repeated cell detachment from solid substrata by enzymatic, chemical or mechanical means. The report here presents a high yield three-dimensional culture and harvest system circumventing the conventional detachment requirements. Cells mixed with dilute cationic collagen were microencapsulated within an ultra-thin shell of synthetic polymers. The cationic collagen could rapidly form a conformal layer of collagen fibers around cells to support cell proliferation and functions. The collagen could be readily removed from cells with a buffer rinse after harvesting from the fragile microcapsules. The cells harvested from this system demonstrate improved attachment, morphology and functions over conventionally cultured cells, upon binding to ligand-conjugated polymer surfaces. The harvested cells can be re-encapsulated and allowed to proliferate again, or used immediately in applications.
Animals↗
CXCL14 is a novel biomarker for mast cell infiltration in the melanoma tumor microenvironment.
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Letter↗
Impact of inflammatory disease on the nerve microenvironment.
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Animals↗
Conformation biases of amino acids based on tripeptide microenvironment from PDB database.
We have constructed a bank (FTTP) of tendentious factors of three states of three-peptide units from PDB database based on conformational dihedral angle library and demonstrated that amino acid biases toward protein secondary structure are present in natural protein sequences. Our research results reveal that 20 standard amino acids fall into three groups: nine residues inclined to alpha-helix with a common character (e.g. direct side chain aliphatic residues or positive/negative charged residues) arrange in three grades, viz EA, QKRLD, and MN, in turn; seven residues are apt to beta-strand with 2'-branched side chain aliphatic residues or benzyl-included residues, namely PV, IYTC, and F, in three ranks; and four residues SHWG show a double tendency to both alpha and beta. Noticeably, proline has the strongest ability to form extended conformation, especially the Re value up to 9.5298 at position 3 (Table 3). Thus, biases of codons show an evident tendency in protein folding, where GC-rich codons are mainly in charge of forming contracted conformation, especially the codon's first letter plays a dominant role in translating the genomic GC signature into protein sequences and structures. So, biases of amino acids will play an important role in protein folding, folding codons, refining domain, structure prediction, and structural genomics/proteomics.
Amino Acids↗
Initial characterization of the microenvironment that regulates connective tissue degradation in amniochorion during normal human labor.
Extracellular matrix degradation in fetal membranes leading to its rupture is coupled to myometrial activity and cervical ripening during human normal labor. Mechanisms which modulate collagen degradation in amniochorion during labor have not been elucidated. Initial characterization of the effect of different blood compartments on connective tissue degradation in amniochorion during human labor was explored. Amniochorion explants were stimulated with plasma of maternal venous blood, umbilical cord blood or placental blood, obtained from women with pregnancies at term, with or without labor. MMP-2 and MMP-9 activities were quantified in conditioned media by gelatin-zymography as an index of connective tissue degradation. Collagen content was measured in tissue explants and collagen fibrils distribution was examined by electron microscopy. Placental plasma from term pregnancies, with or without labor, is enriched with soluble signals that enhance the in vitro MMP-9 production by amniochorion. Accompanying ultrastructural distortion of collagen fibers and demonstration of collagen degradation fragments confirmed induction of extracellular matrix degradation. Control experiments in which MMP-9 activity was blocked with TIMP-1 resulted in inhibition of all the above mentioned changes. These results suggest that placental intervillous space is a functional compartment in which mediators capable to induce collagen degradation in amniochorion are selectively expressed during human labor.
Amnion↗
Role of epididymal receptor HE6 in the regulation of sperm microenvironment.
HE6 (GPR64) is a highly conserved, tissue-specific heptahelical receptor of the human epididymis. The seven transmembrane (TM7) domains are a hallmark of G-protein-coupled receptors (GPCRs) which have a proven history of being excellent therapeutic targets. Of all currently marketed drugs, >30% are modulators of specific heptahelical receptors, emphasizing the potential of HE6 as a target for pharmaceutical intervention. Targeted mutation of the mouse HE6 counterpart resulted in male infertility, further emphasizing its role as a candidate target for male contraception. However, the precise function of HE6, together with its potential ligand(s), and signal transduction pathways have remained largely unknown. On the basis of shared sequence motifs within the TM7 region, HE6 has been grouped into the B class of GPCRs. Within this class, HE6 belongs to the 'large N-termini' family-B seven-transmembrane (LNB-TM7) receptors, also termed the adhesion-GPCRs. Members of this subgroup are 'orphan' receptors, and they all seem to be cleaved within a conserved GPCR proteolytic site (GPS) domain. The biological significance of the two-subunit architecture is still unknown. Clues to the function of HE6 within the epithelium of male excurrent ducts may come from its co-localisation with the apical actin cytoskeleton and from the down-regulation in "knockout" male mice of various proteins specific to the initial segment.
Amino Acid Sequence↗
Partitioning of quencher ions in the micellar microenvironment of polyoxyethylene nonyl phenol.
This paper has explored the quenching of fluorescence of the dye safranine T (ST) by the inorganic cations viz Cu2+, Co2+, Ni2+ and Mn2+ in micellar solutions of the surfactant dioxyethylene nonyl phenol (Igepal CO-210), pentaoxyethylene nonyl phenol (Igepal CO-520) and dodecaoxyethylene nonyl phenol (Igepal CO-720). The quenching results have been calculated in light of stern volmer equation (SV) to evaluate the extent of interaction between the fluorophore (ST) and quencher. The average concentration of the quencher ions in the micelle have been determined. The quenching efficiency of ST by inorganic ions in micellar medium is lower than that in aqueous medium. The results show that the ions get partitioned in the micellar medium. The values of the partition coefficient of the ions decrease with increase in HLB value and number of oxyethylene groups in Igepal.
Cobalt↗
Cathepsin B and tumor proteolysis: contribution of the tumor microenvironment.
Tumor-stromal interactions induce expression of matrix metalloproteinases and serine proteases and, as shown recently, the cysteine protease cathepsin B. We speculate that such interactions upregulate the transcription factor Ets1, resulting in increased cathepsin B expression. This would be consistent with the observed concomitant upregulation of matrix metalloproteinases and serine proteases as well as with the ability of extracellular matrices and their binding partners to alter cathepsin B expression and secretion. Using a confocal assay to analyze the contribution of tumor-stromal interactions to proteolysis, we have been able to confirm enhanced degradation of extracellular matrices by all three classes of proteases.
Animals↗
Oxidative stress, redox, and the tumor microenvironment.
Cellular metabolism is critical for the generation of energy in biological systems; however, as a result of electron transfer reactions, reactive oxygen species (ROS) are generated in aerobic cells. Although low amounts of ROS are easily tolerated by the cell, abnormally high levels of ROS induce oxidative stress. ROS are also produced after exposure to ionizing radiation, selected chemotherapeutic agents, hyperthermia, inhibition of antioxidant enzymes, or depletion of cellular reductants such as NADPH and glutathione. Oxidative stress such as ionizing radiation produces a variety of highly reactive free radicals that damage cells, initiate signal transduction pathways, and alter gene expression. Cells are capable of countering the effects of oxidative stress by virtue of a complex redox buffering system. With respect to the radiation treatment of cancer, components of the cellular redox armamentarium may be targeted to enhance cell killing in the case of tumors and/or protection in the case of normal tissues.
Animals↗
The human tumor microenvironment: invasive (needle) measurement of oxygen and interstitial fluid pressure.
Invasive needle-based assessments of the extracellular environment in human tumors have yielded important prognostic information that has shaped the direction of future translational research and begun to influence clinical practice. This review focuses on electrode measurements of oxygenation in human tumors, particularly in relation to the practicalities of applying these techniques in the clinic and the relationship to patient outcome. Elevated tumor interstitial fluid pressure (IFP) has been shown to be an important independent prognostic factor in cervix cancer. The pathophysiology of elevated IFP is discussed, along with possible explanations for the strong influence on patient outcome and directions for future research.
Cell Hypoxia↗
Bone marrow mesenchymal stem cells differentiate into functional cardiac phenotypes by cardiac microenvironment.
Heart attacks and congestive heart failure remain among the world's most prominent health challenges despite the many breakthroughs. Bone marrow mesenchymal stem cells (BMSCs) have the potential to transdifferentiate into myocytes if an appropriate cardiac environment is provided. This study is meant to investigate the ability of BMSCs to differentiate into cardiomyocytes in a conditioned medium. BMSCs were isolated from rat femurs and tibias using Percoll gradient centrifugation method. Cells were expanded as undifferentiated cells in culture for more than 3 passages and their phenotypes were identified with flow cytometer. BMSCs were cocultured with neonatal rat ventricular myocytes in a rate of 1:10 separated by semipermeable membrane. BMSCs marker of CD29 were highly expressed (98.89+/-1.2%); however, CD34 could hardly be identified (5.61+/-0.1%). After coculturing with myocytes, some of BMSCs showed contraction which became more regular and more vigorous. As assessed by RT-PCR, SERCA2 and RyR(2) were expressed by newly formed cells from 1 to 3 weeks. Immunostaining of newly differentiated BMSCs revealed positivity for cTnT. Some of these cells were positive for sarcomeric alpha-actinin, desmin, cTnT, and cTnI. Western blotting showed that cTnI protein expression was upregulated in these cells from 1 to 3 weeks. Newly formed BMSCs exhibited ultrastructural features of sarcomere formation and inward rectifier potassium current (I(K1)). It is concluded that BMSCs possess the potential to differentiate into cardiomyocytes in the cardiac environment. BMSCs provide an excellent model for development of stem cell therapeutics, and their potential in the cardiac repair under various pathological conditions.
Animals↗
Role of microenvironment in trophoblastic tissue growth and invasion.
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Animals↗
Renal fibrosis. Extracellular matrix microenvironment regulates migratory behavior of activated tubular epithelial cells.
During progression of chronic renal disease, qualitative and quantitative changes in the composition of tubular basement membranes (TBMs) and interstitial matrix occur. Transforming growth factor (TGF)-beta(1)-mediated activation of tubular epithelial cells (TECs) is speculated to be a key contributor to the progression of tubulointerstitial fibrosis. To further understand the pathogenesis associated with renal fibrosis, we developed an in vitro Boyden chamber system using renal basement membranes that partially mimics in vivo conditions of TECs during health and disease. Direct stimulation of TECs with TGF-beta(1)/epithelial growth factor results in an increased migratory capacity across bovine TBM preparations. This is associated with increased matrix metalloproteinase (MMP) production, namely MMP-2 and MMP-9. Indirect chemotactic stimulation by TGF-beta(1)/EGF or collagen type I was insufficient in inducing migration of untreated TECs across bovine TBM preparation, suggesting that basement membrane integrity and composition play an important role in protecting TECs from interstitial fibrotic stimuli. Additionally, neutralization of MMPs by COL-3 inhibitor dramatically decreases the capacity of TGF-beta(1)-stimulated TECs to migrate through bovine TBM preparation. Collectively, these results demonstrate that basement membrane structure, integrity, and composition play an important role in determining interstitial influences on TECs and subsequent impact on potential aberrant cell-matrix interactions.
Adult↗
In situ characterization of genetically targeted (green fluorescent) single cells and their microenvironment in an adoptive host.
Stable expression of transgene-encoded enhanced green fluorescence protein (eGFP) was used as a sensitive and specific marker to detect in situ donor cells engrafted into different tissues of adoptive hosts. eGFP(+) lymphoid or myeloid cells (eg, CD4(+) T cells or bone marrow-derived dendritic cells) from eGFP-transgenic C57BL/6 donor mice were injected into congenic, immunodeficient RAG1(-/-) C57/BL6 hosts. eGFP(+) cells were detected in the adoptive host from 2 days to 4 weeks after transfer using an optimized method of fixed cryopreservation to process the tissue. This allowed the simple, sensitive, and specific detection of eGFP(+) donor cells in histological sections of transplanted hosts. We further demonstrate that this technique can be combined with other established labeling methods such as 1) immunofluorescent labeling to characterize the host cells interacting with engrafted cells and to determine the phenotype of the engrafted cells in situ; 2) terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining to detect apoptotic death of engrafted and autochthonous cell populations; and 3) fluorescent antibody labeling of incorporated bromodeoxyuridine to measure the fraction of proliferating cells in the graft.
Adoptive Transfer↗
Alteration of protease expression phenotype of mouse peritoneal mast cells by changing the microenvironment as demonstrated by in situ hybridization histochemistry.
Mouse mast cell protease (MMCP) mRNA expression was examined by in situ hybridization histochemistry. Peritoneal mast cells (PMCs) of WBB6F1-(+/+) mice expressed MMCP-2, MMCP-4, MMCP-5, and MMCP-6 mRNAs, but did not express MMCP-1 mRNA. When proliferation of PMCs was induced by culturing them in methylcellulose with T cell-derived cytokines, cells in mast cell colonies expressed MMCP-1 mRNA. These mast cells were transferred to a suspension culture to induce further proliferation. The phenotype of the resulting PMC-derived cultured mast cells was similar to that of bone marrow-derived cultured mast cells. When 10(5) PMC-derived cultured mast cells or 10(5) bone marrow-derived cultured mast cells were injected into the stomach wall of mast cell-deficient WBB6F1-W/Wv mice, mast cells that appeared in the mucosa and muscularis propria were similar to mast cells in the stomach of intact WBB6F1-(+/+) mice, indicating the injected cells adapted to a new tissue environment. In contrast, when 10(5) PMCs were injected into the stomach wall of WBB6F1-W/Wv mice, the injected PMCs did not adapt to the mucosa. When 20 PMCs were injected, they proliferated and adapted to the mucosal environment. The present results suggest that PMCs adapt to new environments when proliferation occurs before redifferentiation.
Animals↗
Changes in membrane microenvironment and signal transduction in platelets from NIDDM patients-a pilot study.
BACKGROUND: Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by the presence of abnormally active platelets in the circulation, leading to increased incidence of thrombotic complications. In this study, we have attempted to understand the pathophysiology of the platelets in NIDDM. METHODS: Platelet aggregation was induced by thrombin receptor-activating peptide or epinephrine. Membrane fluidity was derived from the steady-state fluorescence anisotropy of diphenylhexatriene incorporated in the membrane. The phosphotyrosine content of the platelet proteins was probed using specific monoclonal antibodies. The extent of calpain activity was assessed from the proteolysis of calpain substrates. RESULTS: Aggregation was significantly enhanced (p<0.001) in the platelets obtained from the cases of NIDDM. Anisotropy measurements reflected a significant increase in the microviscosity of platelet membranes from 3.315 (+/-0.103) in the control to 4.153 (+/-0.119) in NIDDM. Proteins of relative mobilities of 131, 100, 47 and 38 kDa were found to remain phosphorylated on tyrosine in the resting platelets obtained from NIDDM patients, while they were not phosphorylated in the control counterparts. This was associated with heightened activity of the calcium-dependent thiol protease, calpain, in NIDDM. CONCLUSIONS: Taken together, these data indicated significant changes in the signaling mechanism in the platelets obtained from NIDDM, which could lead to platelet hyperactivity in this disease.
Adult↗
Microenvironment and phenotypic stability specify tissue formation by human articular cartilage-derived cells in vivo.
During in vitro expansion, adult human articular cartilage-derived cells (HACDC) lose their phenotypic stability and capacity to form cartilage in vivo after 4-6 population doublings (PD). Nevertheless, HACDC can be efficiently expanded for up to 20 PD. Here we show that HACDC can generate cartilage, fibrous tissue, skeletal muscle, bone, and adipocytes depending on the balance between phenotypic stability and environmental cues. When 5 x 10(6) cells were injected intramuscularly into nude mice, early-passage (EP)-HACDC formed cartilage; late-passage (LP)-HACDC formed mostly fibrous tissue, but a limited number of cells contributed to muscle formation. When 0.5 x 10(6) cells were injected into regenerating mouse muscle, both EP- and LP-HACDC integrated with host myofibers and expressed muscle genes, but a number of EP-HACDC maintained collagen type II expression. HACDC seeded into Collagraft and implanted subcutaneously into nude mice formed scattered bone islands displaying immunoreactivity for human osteocalcin, and expressing human bone-specific genes. Importantly, neither collagen type II transcript nor cartilage tissue was detected at 8 weeks after implantation. Myogenic, osteogenic, and adipogenic differentiation was induced in vitro using specific culture conditions. These findings provide evidence that in vivo tissue formation by HACDC is specified by a balance between environmental cues and the inherent phenotypic stability.
Adipocytes↗