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PubMed1995

Expression of biologically active basic fibroblast growth factor by genetically modified rat primary skin fibroblasts.

Basic fibroblast growth factor (FGF-2) is normally expressed as a cell-associated protein, and accordingly it is not clear how it exerts its action on target cells in vivo. It has been proposed that cells release, by death or other mechanisms, small amounts of FGF-2 that then acts in an autocrine manner. To address the question of whether it is necessary that FGF-2 remain cell associated or needs to be secreted from cells to have biological activity, we expressed the 18-kDa form of FGF-2 in primary fibroblasts as a cell-associated (FGF-2-B) or as a secreted (FGF-2-S) protein. FGF-2 protein is detected in cell lysates and membrane fractions of both cell types, whereas it is present in significant amounts only in the conditioned medium of FGF-2-S cells. No FGF-2 is detected in control (untransfected) cells. FGF-2-S cells also grow faster than the control of FGF-2-B cells. Yet, when evaluated for their ability to promote the survival of embryonic hippocampal neurons in vitro, both the cell types are active, establishing the activity of the transgene product. We conclude that FGF-2 is active when engineered to be expressed as a cell-associated form or secreted from cells.

Animals↗
PubMed1992

Regulation of the Egr-1 gene by tumor necrosis factor and interferons in primary human fibroblasts.

Treatment of quiescent primary human fibroblasts with tumor necrosis factor (TNF) alpha, TNF-beta, interleukin-1, interferon (IFN) alpha, IFN beta, or IFN gamma induced Egr-1 mRNA. In primary human fibroblasts TNF-alpha and TNF-beta were mildly mitogenic and IFN alpha and IFN gamma were growth inhibitory. However, in HeLa cells TNF but not IFN induced the expression of Egr-1 mRNA, while both cytokines inhibited HeLa cell division. Kinetic measurements of Egr-1 gene expression showed that TNF-alpha, TNF-beta, and IFN gamma increased the cellular concentration of Egr-1 mRNA within 30 min. A maximum induction of Egr-1 mRNA was detected at approximately 60 min which dropped to basal level by 180 min. Induction was inhibited by H7 and staurosporine but not by HA1004, indicating the involvement of a functional protein kinase C. The Egr-1 message was translated and the cellular Egr-1 protein detected within 60 min of cytokine treatment. Despite similar Egr-1 mRNA induction, the amount of Egr-1 protein translated in IFN alpha- and IFN gamma-treated cells was lower than in those treated with TNF-alpha and TNF-beta, and highest in the EGF-treated primary human fibroblasts. Indeed, the level of Egr-1 protein translated in these cells correlated proportionally with both the phosphorylation of cap-binding protein (eukaryotic initiation factor) and the amount of cellular DNA synthesis in the variously treated fibroblasts. These results suggest that both growth stimulatory and inhibitory cytokines can regulate Egr-1 gene expression at the transcriptional and translational level. However, the combination of these regulatory controls may determine the cellular concentration of the Egr-1 gene product and hence, its effect on cell proliferation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1998

Small intestinal submucosa: a substrate for in vitro cell growth.

The extracellular matrix (ECM) of the small intestinal submucosa (SIS) was harvested by removing the superficial layers of the mucosa and the external muscular layers. The remaining 80 microns thick sheet was disinfected and sterilized by methods which removed all cellular components. The SIS-ECM, retaining its native 3-dimensional microarchitecture and composition, was evaluated for its ability to support in vitro cell growth. Six separate cell types were seeded either alone or in coculture with other cells upon this matrix, grown in selected media, a examined daily for time periods ranging from 48 h to 2 weeks. The six cell types tested were NIH Swiss mouse 3T3 fibroblast, NIH 3T3/j2 fibroblasts, primary human fibroblasts, primary human keratinocytes, human microvascular endothelial cells (HMECs), and an established rat osteosarcoma (ROS) cell line. All cell types showed the ability to attach a proliferate. All fibroblast cell line and the keratinocytes proliferated and/or migrated into the 3-dimensional scaffold of the SIS matrix. The ROS cells and the HMECs were confined in their growth pattern to the surface of the matrix. Coculturing of NIH 3T3/J2 fibroblasts and primary human keratinocytes resulted in a distinctive spatial orientation of the two cell types. The fibroblast populated the mid-substance of the 3-dimensional matrix and the keratinocytes formed an epidermal structure with rete ridge-like formation and stratification when the composite was lifted to an air liquid interface in culture. In summary, SIS provides a substratum with a 3-dimensional scaffold that allows for cell migration and spatial organization. The substratum is suitable for in vitro studies of the interaction between epithelial or mesenchymal cells and a naturally occurring extracellular matrix.

3T3 Cells↗
PubMed1981

Calcium transport and cellular distribution in quiescent and serum-stimulated primary cultures of bone cells and skin fibroblasts.

Primary cultures of bone cells and skin fibroblasts were examined for their Ca++ content, intracellular distribution and Ca++ fluxes. Kinetic analysis of 45Ca++ efflux curves indicated the presence of three exchangeable Ca++ compartments which turned over at different rates: a "very fast turnover" (S1), a "fast turnover" (S2, and a "slow turnover" Ca++ pool (S3). S1 was taken to represent extracellular membrane-bound Ca++, S2 represented cytosolic Ca++, and S3 was taken to represent Ca++ sequestered in some intracellular organelles, probably the mitochondria. Bone cells contained about twice the amount of Ca++ as compared with cultured fibroblasts. Most of this extra Ca++ was localized in the "slow turnover" intracellular Ca++ pool (S3). Serum activation caused the following changes in the amount, distribution, and fluxes of Ca++: (1) In both types of cells serum caused an increase in the amount of Ca++ in the "very fast turnover" Ca++ pool, and an increase in the rate constant of 45Ca++ efflux from this pool, indicating a decrease in the strength of Ca++ binding to ligands on cell membranes. (2) In fibroblasts, serum activation also caused a marked decrease in the content of Ca++ in the "slow turnover" Ca++ pool (S3), an increase in the rates of Ca++ efflux from the cells to the medium, and from S3 to S2, as well as a decrease in the rate of influx into S3. (3) In bone cells the amount of Ca++ in S3 remained high in "serum activated" cells, the rate of efflux from S3 to S2 increased, and the rate of influx into S3 also increased. The rate of efflux from the cells to the medium did not change. The results suggest specific properties of bone cells with regard to cell Ca++ presumably connected with their differentiation. Following serum activation we investigated the time course of changes in the amount of exchangeable Ca++ in bone cells and fibroblasts, in parallel with measurements of 3H-thymidine incorporation and cell numbers. Serum activation caused a rapid decrease in the content of cell Ca++ which was followed by a biphasic increase lasting until cell division.

Animals↗
PubMed1975

Secretion of a nerve growth factor by primary chick fibroblast cultures.

Normal primary chick embryo fibroblast cultures product a nerve growth-promoting factor which cross-reacts with monospecfic antibody to pure male mouse submaxillary gland nerve growth factor (NGF). When taken together with the earlier demonstration that mouse L2 CELLS AND 3T3 cells also produce an NGF-like protein, these findings suggest that secretion of this factor may be a general property of fibroblast.

Animals↗
PubMed2005

Platelet-derived growth factor and reactive oxygen species (ROS) regulate Ras protein levels in primary human fibroblasts via ERK1/2. Amplification of ROS and Ras in systemic sclerosis fibroblasts.

The levels of Ras proteins in human primary fibroblasts are regulated by PDGF (platelet-derived growth factor). PDGF induced post-transcriptionally Ha-Ras by stimulating reactive oxygen species (ROS) and ERK1/2. Activation of ERK1/2 and high ROS levels stabilize Ha-Ras protein, by inhibiting proteasomal degradation. We found a remarkable example in vivo of amplification of this circuitry in fibroblasts derived from systemic sclerosis (scleroderma) lesions, producing vast excess of ROS and undergoing rapid senescence. High ROS, Ha-Ras, and active ERK1/2 stimulated collagen synthesis, DNA damage, and accelerated senescence. Conversely ROS or Ras inhibition interrupted the signaling cascade and restored the normal phenotype. We conclude that in primary fibroblasts stabilization of Ras protein by ROS and ERK1/2 amplifies the response of the cells to growth factors and in systemic sclerosis represents a critical factor in the onset and progression of the disease.

Apoptosis↗
PubMed2000

Loss of wild-type p53 function is responsible for upregulated homologous recombination in immortal rodent fibroblasts.

PURPOSE: A correlation between mutations in the tumour suppressor gene p53 and high rates of homologous recombination were previously found in immortal rodent fibroblasts. In the current study, direct evidence was sought that loss of p53 function is mainly responsible for upregulated levels of homologous recombination. MATERIALS AND METHODS: Homologous recombination was assessed in vitro using DNA plasmid substrates that stably integrated into the genome of mouse and rat embryonic fibroblasts. RESULTS: Primary fibroblasts with wild-type p53 displayed a recombination rate of about 1 x 10(-4). This number increased by 33- to 93-fold after spontaneous cellular immortalization, accompanied by loss of p53 function. To exclude potential bias from other gene mutations, wild-type p53 was experimentally disrupted in primary fibroblasts leading to an increase in recombination by one order of magnitude. Conversely, re-introduction of wild-type p53 into p53-null immortal cells reconstituted suppressed recombination rates. Finally, early-passage fibroblast cultures from p53-knock-out mice showed elevated recombination rates, which did not increase further following immortalization. CONCLUSIONS: Loss of wild-type p53 is the major genetic determinant of increased homologous recombination frequencies in immortal rodent fibroblasts. Cellular p53 status will be an important factor to consider when performing functional analysis of the increasing number of mammalian proteins that are found to be involved in homologous recombination.

Animals↗
PubMed1999

Cytocompatibility of periodontal dressing materials in fibroblast and primary human osteoblast-like cultures.

Purpose of this investigation was to determine the cytocompatibility of various periodontal dressing materials by means of human primary gingival fibroblasts (HGF), human osteoblast-like cells (HObl) derived from the alveolar bone, and permanent 3T3 mouse fibroblasts (3T3). Cell culture medium extracts (time periods of extraction: day 1 and between day 2 and day 8 after setting) as well as solid specimens of the following materials were investigated: Coe-pak, Voco pac, Peripac, and Barricaid. Responses of cultures exposed for 24 h and 48 h to these materials were monitored by the fluorescent dyes H33342 and sulforhodamin 101 as well as by light microscopy. It was found that most extracts of Voco pac, Peripac, and Barricaid did not inhibit growth of HGF. Coe-Pak, however, clearly reduced the proliferation of HGF compared to untreated controls. Peripac decreased growth of HObl whereas Coe-Pak, Voco pac, and Barricaid caused no cytotoxic alterations in any of the test assays. Contrary to HGF and HObl, 3T3 cells were much more irritated by the test materials. But the light-curing resinous material Barricaid reduced proliferation of 3T3-fibroblasts only slightly. Our data indicate that Barricaid is exceedingly cytocompatible, whereas all other materials revealed moderate or severe cytotoxic effects according to the cell type.

3T3 Cells↗
PubMed1996

Acidic fibroblast growth factor enhances peroxynitrite-induced apoptosis in primary murine fibroblasts.

Oxidative stress is considered a major mediator of apoptosis in several cellular systems. Peroxynitrite is a highly toxic oxidant formed by the reaction of nitric oxide with superoxide. Primary embryonic murine fibroblasts, exposed to 1 mM peroxynitrite, resulted in delayed cell death characterized by membrane blebbing, cytoplasmic shrinkage, nuclear condensation, and DNA fragmentation that were more characteristic of apoptosis than necrosis. In addition, both morphological alterations and DNA fragmentation were inhibited by the endonuclease inhibitor aurintricarboxylic acid. Pretreatment of fibroblasts with acidic fibroblast growth factor (FGF-1) markedly enhanced peroxynitrite-induced apoptosis, an observation restricted to immediate-early transcriptional and activated tyrosine phosphorylation processes. FGF-1 pretreatment had no modulatory effect on cell death elicited by other reactive oxygen species, suggesting that enhancement of apoptosis involves a unique relationship between peroxynitrite and the growth factor. Exposure of cells to peroxynitrite resulted in immediate tyrosine nitration of several polypeptides, including major targets with estimated molecular masses of 62, 68, and 77 kDa. Pretreatment with FGF-1 did not alter targets of peroxynitrite-mediated tyrosine nitration, but rather increased the total amount of this amino acid modification. Treatment with other reactive oxygen species failed to induce tyrosine nitration. Collectively, these efforts demonstrate that FGF-1 transiently renders primary fibroblasts more sensitive to peroxynitrite-induced apoptosis. In addition, results presented here predict a pivotal role for FGF-1 and peroxynitrite-induced cytotoxicity during the resolution of inflammation and repair processes in vivo.

Animals↗
PubMed1997

Cell-specific in vivo DNA-protein interactions at the proximal promoters of the pro alpha 1(I) and the pro alpha2(I) collagen genes.

We performed in vivo dimethylsulfate footprinting of the 220 bp mouse proximal proalpha1(I) collagen promoter and the 350 bp mouse proximal proalpha2(I) collagen promoter in BALB/3T3 fibroblasts, primary mouse skin fibroblasts, S-194 B cells, NMuLi liver epithelial cells and RAG renal adenocarcinoma cells and in vitro DNase I footprinting of these promoters using nuclear extracts of these different cell types. Whereas proalpha1(I) and proalpha2(I) collagen RNAs were present in BALB/3T3 fibroblasts and primary fibroblasts, these RNAs could not be detected in the three other cell lines. Comparison of in vitro DNase I footprints for each of the two proximal collagen promoters indicated that the patterns of protection were very similar with the different nuclear extracts, suggesting that the DNA binding proteins binding to these promoters were present in all cell types tested. In contrast, in vivo footprints over these proximal promoters were cell-specific, occurring only in fibroblast cells and not in the other three cell types. The in vivo footprints were generally located within the in vitro footprinted regions. Our results suggest that although all cell types tested contained nuclear proteins that can bind to the proximal proalpha1(I) and proalpha2(I) collagen promoters in vitro , it is only in fibroblasts that these proteins bind to their cognate sites in vivo . We discuss possible regulatory mechanisms in type I collagen genes that can contribute to the cell-specific in vivo protein-DNA interactions at the proximal promoters.

3T3 Cells↗
PubMed1992

Morphological and neurochemical features of cultured primary skin fibroblasts of Fischer 344 rats following striatal implantation.

In order to assess the feasibility of using primary skin fibroblasts as a donor population for genetic modification and subsequent intracerebral grafting, the present study examines the structural and neurochemical characteristics of intrastriatal grafts of isogeneic primary fibroblasts over a period of 6 months. In culture, primary skin fibroblasts obtained from a female Fischer 344 rat display robust growth, but once confluent these cells exhibit contact inhibition. Following the implantation of cultured primary cells within the striatum of other adult rats from the same inbred strain, isologous grafts stain immunohistochemically for fibronectin at 1 week, and this immunostaining persists up to 6 months. Immunoreactivity for laminin is intense within the grafts from 1 to 8 weeks, but decreases by 6 months. Astrocytes within the striatum respond dramatically to the implantation of primary fibroblasts, such that immunohistochemical staining for glial fibrillary acidic protein increases markedly from 1 to 8 weeks after implantation. Although the intensity of immunostaining for glial fibrillary acidic protein diminishes among striatal astrocytes between 8 weeks and 6 months, the astrocytic border between the grafts and striatal neuropil remains intensely immunoreactive. Capillaries within the grafts stain immunohistochemically for glucose transporter (a facilitated glucose uptake carrier) as early as 3 weeks after implantation. Following intravenous infusions of peroxidase, capillaries within fibroblast grafts do not permit the extravasation of this macromolecule at 8 weeks and 6 months. Thus, capillaries formed within intracerebral grafts of primary skin fibroblasts exhibit a functional impermeable barrier to macromolecules similar to those capillaries of the host striatum. At the ultrastructural level, grafts possess numerous fibroblasts and have an extracellular matrix filled with collagen. Reactive astrocytic processes filled with intermediate filaments are found throughout the grafts. Hypertrophied astrocytes and their processes also appear to form a continuous border between the grafts and striatal neuropil. Grafts of primary fibroblasts also possess an extensive vasculature that is composed of capillaries with nonfenestrated endothelial cells; the occurrence of reactive astrocytic processes closely associated with or enveloping capillaries is variable. These results provide direct morphological and neurochemical evidence for the long-term survival of isologous fibroblasts after implantation within the rat striatum. From these data, we propose that isologous skin fibroblasts can be considered as donor candidates for successful intracerebral grafting following gene transfer.

Animals↗
PubMed1988

Phenotypic transformation of primary mouse fibroblasts by BPV 1 DNA.

Cultures of primary fibroblasts of C57BL/6J mice were used as targets for transformation by bovine papillomavirus type 1 (BPV 1) DNA. Although no foci were observed, several lines of transformed cells were established by subculturing. These immortalized cell lines had in vitro growth characteristics in high and low serum media and saturation densities typical of transformed cells. Karyotype analyses revealed extensive aneuploidic changes. In two of the three cell lines analyzed, viral DNA was present in monomeric episomal form, in the third cell line all viral sequences were found in the high molecular weight region of a Southern blot. Despite the transformed phenotype, only one of the cell lines was tumorigenic in nude mice at a low level.

Animals↗
PubMed2004

Prevention of experimental autoimmune encephalomyelitis in DA rats by grafting primary skin fibroblasts engineered to express transforming growth factor-beta1.

To determine whether primary fibroblasts producing latent transforming growth factor beta1 (TGF-beta1) are capable of down-regulating experimental autoimmune encephalomyelitis (EAE), a retroviral vector TGF-beta1-pBabe-neo (-5'UTR) was used for efficient gene transfer into primary skin fibroblasts of DA rats. After heat activation, conditioned medium from the transduced fibroblasts was found to inhibit significantly in vitro proliferation of lymphocytes from lymph nodes of DA rats with EAE. Intraperitoneal administration of TGF-beta1-transduced fibroblasts into DA rats during the priming phase of EAE resulted in a significant reduction in mortality and in the mean clinical and EAE scores versus the control immunized animals treated with non-transduced fibroblasts.

Animals↗
PubMed1988

The influence of synovial fluids from patients with rheumatic diseases on chick embryo fibroblasts.

Primary chick-embryo fibroblasts (PCEF) were used as target cells to measure the influence of synovial fluids of patients suffering from osteoarthritis (OA; n = 5), rheumatoid arthritis (RA; n = 12) and psoriatic arthritis (PA; n = 2). The following metabolic cell products were measured: DNA, RNA, glycosaminoglycans (GAG), sulfated glycosaminoglycans, protein and collagen, with the same joint effusions being used in each test. Since it is not a single substance that provokes a stimulating or inhibiting effect in the joint, the crude synovial fluids were applied in these preliminary experiments. It was found that each type of synovial fluid showed an influence on the biological processes in the PCEF. The DNA, RNA and GAG syntheses were strongly influenced by the joint effusions, in contrast to the protein, collagen and sulfated glycosaminoglycan syntheses which were less affected. Generally, the nucleic acid synthesis differed significantly between the OA, RA and PA synovial fluids. The addition of heparin to the synovial fluids caused an additive inhibiting effect on the DNA synthesis but did not influence the other biochemical parameters. The synovial fluids of RA patients, and to a much greater extent those of PA patients, inhibited the thymidine incorporation whereas OA synovial fluids had a less pronounced effect. This result indicates a disease-dependent composition of the synovial fluids. RNA synthesis was diminished in all three groups, but again this effect was strongest in the case of the PA synovial fluids. GAG synthesis was markedly stimulated by the PA synovial fluids and somewhat, though to a lesser extent, by the OA and RA synovial fluids. The sulfated glycosaminoglycan synthesis in the PCEF, as revealed by 35S incorporation into the GAG, was less influenced and on the whole stimulated by the OA and RA synovial fluids. The same trend could be observed with regard to the collagen synthesis. The intracellular protein synthesis was less influenced by the OA (91.9%) and more strongly suppressed by the RA (78.7%) and the PA (76.7%) synovial fluids. PCEF therefore appear to be a convenient and sensitive target cell system to study alterations of biochemical processes caused by crude synovial fluids and also of different origin by individual factors isolated from synovial fluids.

Animals↗
PubMedDate not supplied

Defective repair of UV-induced DNA damage in cultured primary skin fibroblasts from Saudi thyroid cancer patients.

This study was conducted to examine the sensitivity of primary skin fibroblasts from Saudi thyroid cancer (TC) patients to ultraviolet (UV) irradiation. Cell survival was studied by a colony forming assay and DNA repair defects with a host cell reactivation (HCR) assay using UV-irradiated Herpes Simplex Virus (HSV). In addition, p53 gene expression was examined in the same TC cells exhibiting enhanced radiosensitivity. Skin fibroblasts from TC patients (n=4) showed significantly enhanced sensitivity to UV radiation. The average UV dose to reduce survival to 37% of the initial survival (D(37)) value (in Jm(-2)) for fibroblasts from TC patients was 4.6 (3.7-5.6) compared to 7.3 (6.3-8.3) for healthy individuals (n=3). UV-sensitive xeroderma pigmentosum (XP) cells, which were used as positive control, were found to be extremely sensitive with a D(37) value of 0.6 Jm(-2). In a host cell reactivation assay, UV-irradiated HSV was tested for its plaque-forming ability (PFA), by plating infected fibroblasts from TC patients (used as host cells) on African Green Monkey (Vero) kidney cells to form plaques. A significant reduction in the PFA of the UV-irradiated virus (about three fold) on TC cells compared to fibroblasts from the healthy subjects was seen, suggesting a DNA-repair deficiency in the primary fibroblasts of the TC patients. Furthermore, no significant accumulation in radiation-induced p53 expression was observed in cells from the TC patients. Our results, based on a relatively small group of subjects, indicate that Saudi TC patients primary fibroblasts (non-cancerous in nature) may be carriers of cancer-susceptible gene(s) arising from defective DNA repair/processing. These results warrant a larger study to investigate the role of UV-induced bulky DNA damage in thyroid cancer susceptibility.

Apoptosis↗
PubMed2006

Chemosensitivity of primary human fibroblasts with defective unhooking of DNA interstrand cross-links.

Xeroderma pigmentosum (XP) is characterised by defects in nucleotide excision repair, ultraviolet (UV) radiation sensitivity and increased skin carcinoma. Compared to other complementation groups, XP-F patients show relatively mild cutaneous symptoms. DNA interstrand cross-linking agents are a highly cytotoxic class of DNA damage induced by common cancer chemotherapeutics such as cisplatin and nitrogen mustards. Although the XPF-ERCC1 structure-specific endonuclease is required for the repair of ICLs cellular sensitivity of primary human XP-F cells has not been established. In clonogenic survival assays, primary fibroblasts from XP-F patients were moderately sensitive to both UVC and HN2 compared to normal cells (2- to 3-fold and 3- to 5-fold, respectively). XP-A fibroblasts were considerably more sensitive to UVC (10- to 12-fold) but not sensitive to HN2. The sensitivity of XP-F fibroblasts to HN2 correlated with the defective incision or 'unhooking' step of ICL repair. Using the comet assay, XP-F cells exhibited only 20% residual unhooking activity over 24 h. Over the same time, normal and XP-A cells unhooked greater than 95% and 62% of ICLs, respectively. After HN2 treatment, ICL-associated DNA double-strand breaks (DSBs) are detected by pulse field gel electrophoresis in dividing cells. Induction and repair of DNA DSBs was normal in XP-F fibroblasts. These findings demonstrate that in primary human fibroblasts, XPF is required for the unhooking of ICLs and not for the induction or repair of ICL-associated DNA DSBs induced by HN2. In terms of cancer chemotherapy, people with mild DNA repair defects affecting ICL repair may be more prevalent in the general population than expected. Since cellular sensitivity of primary human fibroblasts usually reflects clinical sensitivity such patients with cancer would be at risk of increased toxicity.

Cell Culture Techniques↗
PubMed1983

Relationship of cell growth to collagen synthesis in glucocorticoid treated A/J and C57BL6/J neonatal mouse dermal fibroblasts.

Primary cultures of neonatal dermal fibroblasts from two strains of mice (A/J and C57BL6/J) were utilized as an in vitro system to investigate the effects of glucocorticoids on cell growth and collagen synthesis. Protein and DNA synthesis were lower in untreated (control) A/J fibroblasts than in C57BL6/J fibroblasts. Treatment with glucocorticoids for 4 days resulted in dose-dependent inhibition of [3H]thymidine incorporation into DNA and a reduction in collagen synthesis. Collagen synthesis was differentially more susceptible to glucocorticoids than was total protein synthesis. Neonatal dermal fibroblasts obtained from A/J mice were more sensitive to glucocorticoids than were cells from C57BL6/J mice. Reduction in collagen production by anti-inflammatory steroids in this system may be related to adverse effects observed in vivo following treatment with these steroids.

Animals↗
PubMed1991

[Extracellular matrix in gingival fibroblasts].

Primary cultures of human gingival fibroblasts from patients of different age have been established. Histotype characterization has been confirmed by ultrastructural morphology and by the positivity of intermediate filament vimentin. Extracellular matrix expression has been analyzed by immunocitochemistry. Our data demonstrate that the extracellular matrix of human gingival fibroblasts is composed of type IV collagen, other than fibronectin and type I-III collagens.

Cells, Cultured↗