scholarly journals Co-ordinate increase in the expression of type I and type III collagen genes in progressive systemic sclerosis fibroblasts

1986 ◽  
Vol 237 (3) ◽  
pp. 837-843 ◽  
Author(s):  
S A Jimenez ◽  
G Feldman ◽  
R I Bashey ◽  
R Bienkowski ◽  
J Rosenbloom
Keyword(s):  
Systemic Sclerosis ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Dermal Fibroblast ◽  
Blot Hybridization ◽  
Progressive Systemic Sclerosis ◽  
Dermal Fibroblasts ◽  
Type Iii Collagen ◽  
Type I ◽  
Dot Blot

Progressive systemic sclerosis (PSS), is a connective tissue disease characterized by excessive accumulation of collagen in the skin and various internal organs which is due, at least in part, to increased collagen production by PSS fibroblasts. In order to examine the molecular mechanisms responsible for this abnormality, we compared the kinetics of collagen biosynthesis, the intracellular degradation of collagen and the expression of Types I and III procollagen genes between normal and PSS dermal fibroblasts in culture. Two age- and sex-matched normal and PSS dermal fibroblast cell lines were studied. The results showed that the PSS cultures produced higher amounts of collagen than did normal fibroblasts and displayed an abnormal kinetic pattern. Furthermore, the PSS cells showed a slight but statistically significant increase in the fraction of collagen degraded intracellularly when compared with normal cells (23% against 18% respectively). The levels of mRNA for procollagen Types I and III were determined by Northern and dot-blot hybridization with specific cloned cDNA probes for alpha 1(I), alpha 2(I) and alpha 1(III) and it was found that they were 2-3-fold higher for each of the three chains in the PSS cell lines compared with the controls. These findings indicate, therefore, that the overproduction of collagen characteristic of PSS fibroblasts can be largely accounted for by the increased levels of collagen mRNA.

scholarly journals Modulation by 17,20S(OH)2pD of Fibrosis-Related Mediators in Dermal Fibroblast Lines from Healthy Donors and from Patients with Systemic Sclerosis

2021 ◽  
Vol 23 (1) ◽  
pp. 367
Author(s):  
Monica L. Brown Lobbins ◽  
Andrzej T. Slominski ◽  
Karen A. Hasty ◽  
Sicheng Zhang ◽  
Duane D. Miller ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Type I Collagen ◽  
Dermal Fibroblast ◽  
Positive Control ◽  
Dermal Fibroblasts ◽  
Normal Donor ◽  
Type I ◽  
Collagen Production ◽  
Healthy Donors ◽  
Tgf Β1

We previously demonstrated that the non-calcemic pregnacalciferol (pD) analog 17,20S (OH)2pD suppressed TGF-β1-induced type I collagen production in cultured normal human dermal fibroblasts. In the present studies, we examined fibroblasts cultured from the lesional skin of patients with systemic sclerosis (scleroderma (SSc)) and assessed the effects of 17,20S(OH)2pD on fibrosis-related mediators. Dermal fibroblast lines were established from skin biopsies from patients with SSc and healthy controls. Fibroblasts were cultured with either 17,20S(OH)2pD or 1,25(OH)2D3 (positive control) with/without TGF-β1 stimulation and extracted for protein and/or mRNA for collagen synthesis and mediators of fibrosis (MMP-1, TIMP-1, PAI-1, BMP-7, PGES, GLI1, and GLI2). 1 7,20S(OH)2pD (similar to 1,25(OH)2D3) significantly suppressed net total collagen production in TGF-β1-stimulated normal donor fibroblast cultures and in cultures of SSc dermal fibroblasts. 17,20S(OH)2pD (similar to 1,25(OH)2D3) also increased MMP-1, BMP-7, and PGES and decreased TIMP-1 and PAI1 expression in SSc fibroblasts. Although 17,20S(OH)2pD had no effect on Gli1 or Gli2 in SSc fibroblasts, it increased Gli2 expression when cultured with TGF-β1 in normal fibroblasts. These studies demonstrated that 17,20S(OH)2pD modulates mediators of fibrosis to favor the reduction of fibrosis and may offer new noncalcemic secosteroidal therapeutic approaches for treating SSc and fibrosis.

scholarly journals Acetylated Resveratrol and Oxyresveratrol Suppress UVB-Induced MMP-1 Expression in Human Dermal Fibroblasts

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1252
Author(s):  
Jae-Eun Lee ◽  
Jijeong Oh ◽  
Daeun Song ◽  
Mijeong Lee ◽  
Dongyup Hahn ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Dermal Fibroblast ◽  
Aging Effect ◽  
Inhibitory Effect ◽  
Human Dermal Fibroblast ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Hdf Cells

Resveratrol (RES) and oxyresveratrol (OXYRES) are considered and utilized as active ingredients of anti-aging skin cosmetics. However, these compounds are susceptible to oxidative discoloration and unpleasant odor in solutions, limiting their use in cosmetics. Accordingly, RES and OXYRES were chemically modified to acetylated derivatives with enhanced stability, and their anti-aging effect on the skin and detailed molecular mechanism of their acetylated derivatives were investigated. Acetylated RES and OXYRES lost their acetyl group and exerted an inhibitory effect on H2O2-induced ROS levels in human dermal fibroblast (HDF) cells. In addition, RES, OXYRES, and their acetylated derivatives suppressed UVB-induced matrix metalloproteinase (MMP)-1 expression via inhibition of mitogen-activated protein kinases (MAPKs) and Akt/mTOR signaling pathways. Furthermore, RES, OXYRES, and their acetylated derivatives suppressed type I collagen in TPA-treated HDF cells. Collectively, these results suggest the beneficial effects and underlying molecular mechanisms of RES, OXYRES, and their acetylated derivatives for anti- skin aging applications.

Deregulation of c-myc gene expression in human colon carcinoma is not accompanied by amplification or rearrangement of the gene

1985 ◽  
Vol 5 (8) ◽  
pp. 1969-1976
Author(s):  
M D Erisman ◽  
P G Rothberg ◽  
R E Diehl ◽  
C C Morse ◽  
J M Spandorfer ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Cell Lines ◽  
Blot Hybridization ◽  
Human Colon ◽  
Normal Colonic Mucosa ◽  
Dna Rearrangement ◽  
Dot Blot ◽  
Myc Oncogene ◽  
Elevated Expression ◽  
High Level

The structure and expression of the c-myc oncogene were examined in 29 primary human colon adenocarcinomas. Dot blot hybridization of total RNA showed that 21 tumors (72%) had considerably elevated expression of c-myc (5- to 40-fold) relative to normal colonic mucosa. These data were corroborated by Northern blots of polyadenylated RNA, which showed a 2.3-kilobase transcript. Southern analysis of the c-myc locus in these tumors indicated the absence of amplification or DNA rearrangement in a 35-kilobase region encompassing the gene. In a parallel study, elevated expression of c-myc without amplification or DNA rearrangement was also observed in three of six colon carcinoma cell lines examined; in addition, unlike a normal colon cell line control, these three cell lines exhibited constitutive, high-level expression of the gene during their growth in cultures. These results indicate that elevated expression of the c-myc oncogene occurs frequently in primary human colon carcinomas and that the mechanism involved in the regulation of c-myc expression is altered in tumor-derived cell lines.

scholarly journals Asiaticoside induces cell proliferation and collagen synthesis in human dermal fibroblasts

2015 ◽  
Vol 34 (2) ◽  
pp. 96
Author(s):  
Linda Yuliati ◽  
Etik Mardliyati ◽  
Kusmarinah Bramono ◽  
Hans Joachim Freisleben
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Retinoic Acid ◽  
Collagen Synthesis ◽  
Active Agent ◽  
Dermal Fibroblasts ◽  
Type Iii Collagen ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Type Iii

Background<br />Asiatiocoside, a saponin component isolated from Centella asiatica can improve wound healing by promoting the proliferation of human dermal fibroblasts (HDF) and synthesis of collagen. The skin-renewing cells and type I and III collagen synthesis decrease with aging, resulting in the reduction of skin elasticity and delayed wound healing. Usage of natural active compounds from plants in wound healing should be evaluated and compared to retinoic acid as an active agent that regulates wound healing. The aim of this study was to compare and evaluate the effect of asiaticoside and retinoic acid to induce greater cell proliferation and type I and III collagen synthesis in human dermal fibroblast.<br /><br />Methods<br />Laboratory experiments were conducted using human dermal fibroblasts (HDF) isolated from human foreskin explants. Seven passages of HDF were treated with asiaticoside and retinoic acid at several doses and incubated for 24 and 48 hours. Cell viability in all groups was tested with the MTT assay to assess HDF proliferation. Type I and III collagen synthesis was examined using the respective ELISA kits. Analysis of variance was performed to compare the treatment groups. <br /><br />Results<br />Asiaticoside had significantly stronger effects on HDF proliferation than retinoic acid (p&lt;0.05). The type III collagen production was significantly greater induction with asiaticoside compared to retinoic acid (p&lt;0.05). <br /><br />Conclusion<br />Asiaticoside induces HDF proliferation and type I and III collagen synthesis in a time- and dose-dependent pattern. Asiaticoside has a similar effect as retinoic acid on type I and type III collagen synthesis.

scholarly journals Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro

2020 ◽  
Vol 21 (20) ◽  
pp. 7756
Author(s):  
Jung Hwan Oh ◽  
Fatih Karadeniz ◽  
Chang-Suk Kong ◽  
Youngwan Seo
Keyword(s):  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Nuclear Translocation ◽  
Quinic Acid ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Skin Damage ◽  
Chronological Aging

Cutaneous aging is divided into intrinsic and exogenous aging correspondingly contributing to the complex biological phenomenon in skin. Intrinsic aging is also termed chronological aging, which is the accumulation of inevitable changes over time and is largely genetically determined. Superimposed on this intrinsic process, exogenous aging is associated with environmental exposure, mainly to ultraviolet (UV) radiation and more commonly termed as photoaging. UV-induced skin aging induces increased expression of matrix metalloproteinases (MMPs) which in turn causes the collagen degradation. Therefore, MMP inhibitors of natural origin are regarded as a primary approach to prevent or treat photoaging. This study investigated the effects of 3,5-dicaffeoyl-epi-quinic acid (DEQA) on photoaging and elucidated its molecular mechanisms in UVA-irradiated human dermal fibroblasts (HDFs). The results show that treatment with DEQA decreases MMP-1 production and increases type I collagen production in UVA-damaged HDFs. In addition, treatment of UVA-irradiated HDFs with DEQA downregulates MMP-1, MMP-3 and MMP-9 expression via blocking MAPK-cascade-regulated AP-1 transcriptional activity in UVA-irradiated HDFs. Furthermore, DEQA relieves the UVA-mediated suppression of type I procollagen and collagen expression through stimulating TGF-β/Smad signaling, leading to activation of the Smad 2/3 and Smad 4 nuclear translocation. These results suggest that DEQA could be a potential cosmetic agent for prevention and treatment of skin photoaging.

Cartilage oligomeric matrix protein expression in systemic sclerosis reveals heterogeneity of dermal fibroblast responses to transforming growth factor β

2008 ◽  
Vol 68 (3) ◽  
pp. 435-441 ◽  
Author(s):  
G Farina ◽  
R Lemaire ◽  
P Pancari ◽  
J Bayle ◽  
R L Widom ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Growth Factor ◽  
Mrna Expression ◽  
Cartilage Oligomeric Matrix Protein ◽  
Matrix Protein ◽  
Transforming Growth Factor ◽  
Dermal Fibroblast ◽  
Smooth Muscle Actin ◽  
Dermal Fibroblasts ◽  
Cultured Fibroblasts

Objective:Cartilage oligomeric matrix protein (COMP) accumulates in systemic sclerosis (SSc) skin and is upregulated by transforming growth factor (TGF)β. To further characterise the response to TGFβ in SSc, we investigated TGFβ1 and COMP expression and myofibroblast staining in SSc skin.Methods:Skin biopsies from patients with diffuse cutaneous SSc (dSSc), limited cutaneous SSc (lSSc) and healthy controls were evaluated for COMP mRNA expression using real-time PCR. COMP, α-smooth muscle actin (SMA) and TGFβ were assessed in skin sections and in cultured fibroblasts by immunohistochemistry. Clinical disease status was assessed by the modified Rodnan skin score (mRSS).Results:Myofibroblasts expressing SMA and COMP were found coexpressed in many cells in dSSc dermis, but each also stained distinct cells in the dermis. Cultured SSc dermal fibroblasts also showed heterogeneity for COMP and SMA expression, with cells expressing SMA, COMP, both or neither. TGFβ treatment increased COMP and SMA-expressing cells. COMP mRNA expression in lesional skin from patients with dSSc correlated with the mRSS and TGFβ1 staining.Conclusion:These findings suggest that TGFβ upregulation of COMP and/or SMA expression in subpopulations of fibroblasts contributes to different pathways of fibrosis and that multiple TGFβ regulated genes may serve as biomarkers for the degree of SSc skin involvement.

scholarly journals Investigation of type i and type iii collagens of the lung in progressive systemic sclerosis

1981 ◽  
Vol 24 (4) ◽  
pp. 625-631 ◽  
Author(s):  
Jerome M. Seyer ◽  
Andrew H. Kang ◽  
Gerald Rodnan
Keyword(s):  
Systemic Sclerosis ◽  
Progressive Systemic Sclerosis ◽  
Type I ◽  
Type Iii

scholarly journals Effects of paeonol on proliferation and collagen synthesis of rat cardiac fibroblasts induced by aldosterone

2021 ◽  
Vol 16 (2) ◽  
pp. 42-48
Author(s):  
Qian Xu ◽  
Li Na Wang ◽  
Jing Yi Zhao ◽  
Yan Hong Xiao ◽  
Chao Du
Keyword(s):  
Cell Viability ◽  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Ventricular Remodeling ◽  
Cardiac Fibroblasts ◽  
Neonatal Rat ◽  
Type Iii Collagen ◽  
Type I ◽  
Rt Pcr ◽  
Tgf Β1

The aim of this study was to explore the possible molecular mechanisms of paeonol in preventing ventricular remodeling. The cell viability of neonatal rat cardiac fibroblasts was detected by the method of MTT. RT-PCR and Western blot were used to measure the expression of TGF-β1, type I collagen and type III collagen. After treating the cardiac fibroblasts with paeonol, the cell viability decreased (p<0.01), and the expression of TGF-β1, type I collagen and types III collagen was significantly reduced (p<0.01). Thus, paeonol can inhibit the proliferation of fibroblast cells induced by aldosterone. The molecular mechanism is related to the down-regulation of TGF-β1 and type I and III collagen gene expression.

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