scholarly journals EFFECT OF COLLAGEN I GEL ON APOPTOSIS OF RAT HEPATIC STELLATE CELLS

2013 ◽  
Vol 56 (2) ◽  
pp. 73-79
Author(s):  
Lenka Bittnerová ◽  
Alena Jiroutová ◽  
Emil Rudolf ◽  
Martina Řezáčová ◽  
Jiří Kanta
Keyword(s):  
Hepatic Stellate Cells ◽  
Type I Collagen ◽  
Collagen Gel ◽  
Stellate Cells ◽  
Type I ◽  
Function Type ◽  
Fibrotic Liver ◽  
Normal Rat ◽  
And Function

Activated hepatic stellate cells (HSC) are a major source of fibrous proteins in cirrhotic liver. Inducing or accelerating their apoptosis is a potential way of liver fibrosis treatment. Extracellular matrix (ECM) surrounding cells in tissue affects their differentiation, migration, proliferation and function. Type I collagen is the main ECM component in fibrotic liver. We have examined how this protein modifies apoptosis of normal rat HSC induced by gliotoxin, cycloheximide and cytochalasin D in vitro and spontaneous apoptosis of HSC isolated from CCl4-damaged liver. We have found that type I collagen gel enhances HSC apoptosis regardless of the agent triggering this process.

scholarly journals Collagen overlays can inhibit leptin and adiponectin secretion but not lipid accumulation in adipocytes

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4641
Author(s):  
Sherri L. Christian ◽  
Nikitha K. Pallegar ◽  
Robert J. Brown ◽  
Alicia M. Viloria-Petit
Keyword(s):  
Type I Collagen ◽  
Whole Body ◽  
Type I ◽  
Function Type ◽  
Therapeutic Implications ◽  
Triglyceride Accumulation ◽  
Whole Body Metabolism ◽  
And Function

BackgroundWhite adipose tissue (WAT) is essential for energy storage as well as being an active endocrine organ. The secretion of adipokines by adipocytes can affect whole body metabolism, appetite, and contribute to overall health. WAT is comprised of lipid-laden mature adipocytes, as well as immune cells, endothelial cells, pre-adipocytes, and adipose-derived stem cells. In addition, the presence of extracellular matrix (ECM) proteins in WAT can actively influence adipocyte differentiation, growth, and function. Type I collagen is an abundant fibrous ECM protein in WAT that is secreted by developing adipocytes. However, the extent and overall effect of Type I collagen on adipokine secretion in mature adipocytes when added exogenously has not been established.MethodsWe characterized the effects of Type I collagen overlays prepared using two different buffers on adipocyte physiology and function when added at different times during differentiation. In addition, we compared the effect of collagen overlays when adipocytes were cultured on two different tissue culture plastics that have different adherent capabilities. Triglyceride accumulation was analyzed to measure adipocyte physiology, and leptin and adiponectin secretion was determined to analyze effects on adipokine secretion.ResultsWe found that collagen overlays, particularly when added during the early differentiation stage, impaired adipokine secretion from mature adipocytes. Collagen prepared using PBS had a greater suppression of leptin than adiponectin while collagen prepared using HANKS buffer suppressed the secretion of both adipokines. The use of CellBind plates further suppressed leptin secretion. Triglyceride accumulation was not substantially impacted with any of the collagen overlays.DiscussionAdipokine secretion can be selectively altered by collagen overlays. Thus, it is feasible to selectively manipulate the secretion of adipokines by adipocytesin vitroby altering the composition or timing of collagen overlays. The use of this technique could be applied to studies of adipokine function and secretionin vitroas well as having potential therapeutic implications to specifically alter adipocyte functionalityin vivo.

scholarly journals Collagen overlays can inhibit leptin and adiponectin secretion but not lipid accumulation in adipocytes

2018 ◽  
Author(s):  
Sherri Lynn Christian ◽  
Nikitha K Pallegar ◽  
Robert J Brown ◽  
Alicia M Viloria-Petit
Keyword(s):  
Type I Collagen ◽  
Whole Body ◽  
Type I ◽  
Function Type ◽  
Therapeutic Implications ◽  
Triglyceride Accumulation ◽  
Whole Body Metabolism ◽  
And Function

Background. White adipose tissue (WAT) is essential for energy storage as well as being an active endocrine organ. The secretion of adipokines by adipocytes can affect whole body metabolism, appetite, and contribute to overall health. WAT is comprised of lipid-laden mature adipocytes, as well as immune cells, endothelial cells, pre-adipocytes, and adipose-derived stem cells. In addition, the presence of extracellular matrix (ECM) proteins in WAT can actively influence adipocyte differentiation, growth, and function. Type I collagen is an abundant fibrous ECM protein in WAT that is secreted by developing adipocytes. However, the extent and overall effect of Type I collagen on adipokine secretion in mature adipocytes when added exogenously has not been established. Methods. We characterized the effects of Type I collagen overlays prepared using two different buffers on adipocyte physiology and function when added at different times during differentiation. In addition, we compared the effect of collagen overlays when adipocytes were cultured on two different tissue culture plastics that have different adherent capabilities. Triglyceride accumulation was analyzed to measure adipocyte physiology, and leptin and adiponectin secretion was determined to analyze effects on adipokine secretion. Results. We found that collagen overlays, particularly when added during the early differentiation stage, impaired adipokine secretion from mature adipocytes. Collagen prepared using PBS had a greater suppression of leptin than adiponectin while collagen prepared using HANKS buffer suppressed the secretion of both adipokines. The use of CellBind plates further suppressed leptin secretion. Triglyceride accumulation was minimally impacted with any of the collagen overlays. Discussion. Adipokine secretion can be selectively altered by collagen overlays. Thus, it is feasible to selectively manipulate the secretion of adipokines by adipocytes in vitro by altering the composition or timing of collagen overlays. The use of this technique could be applied to studies of adipokine function and secretion in vitro as well as having potential therapeutic implications to specifically alter adipocyte functionality in vivo.

scholarly journals Collagen overlays can inhibit leptin and adiponectin secretion but not lipid accumulation in adipocytes

2018 ◽  
Author(s):  
Sherri Lynn Christian ◽  
Nikitha K Pallegar ◽  
Robert J Brown ◽  
Alicia M Viloria-Petit
Keyword(s):  
Type I Collagen ◽  
Whole Body ◽  
Type I ◽  
Function Type ◽  
Therapeutic Implications ◽  
Triglyceride Accumulation ◽  
Whole Body Metabolism ◽  
And Function

Background. White adipose tissue (WAT) is essential for energy storage as well as being an active endocrine organ. The secretion of adipokines by adipocytes can affect whole body metabolism, appetite, and contribute to overall health. WAT is comprised of lipid-laden mature adipocytes, as well as immune cells, endothelial cells, pre-adipocytes, and adipose-derived stem cells. In addition, the presence of extracellular matrix (ECM) proteins in WAT can actively influence adipocyte differentiation, growth, and function. Type I collagen is an abundant fibrous ECM protein in WAT that is secreted by developing adipocytes. However, the extent and overall effect of Type I collagen on adipokine secretion in mature adipocytes when added exogenously has not been established. Methods. We characterized the effects of Type I collagen overlays prepared using two different buffers on adipocyte physiology and function when added at different times during differentiation. In addition, we compared the effect of collagen overlays when adipocytes were cultured on two different tissue culture plastics that have different adherent capabilities. Triglyceride accumulation was analyzed to measure adipocyte physiology, and leptin and adiponectin secretion was determined to analyze effects on adipokine secretion. Results. We found that collagen overlays, particularly when added during the early differentiation stage, impaired adipokine secretion from mature adipocytes. Collagen prepared using PBS had a greater suppression of leptin than adiponectin while collagen prepared using HANKS buffer suppressed the secretion of both adipokines. The use of CellBind plates further suppressed leptin secretion. Triglyceride accumulation was minimally impacted with any of the collagen overlays. Discussion. Adipokine secretion can be selectively altered by collagen overlays. Thus, it is feasible to selectively manipulate the secretion of adipokines by adipocytes in vitro by altering the composition or timing of collagen overlays. The use of this technique could be applied to studies of adipokine function and secretion in vitro as well as having potential therapeutic implications to specifically alter adipocyte functionality in vivo.

A Continuous-Discrete Finite Element Model of Angiogenesis That Couples Vessel Growth With Matrix Deformation

2013 ◽  
Author(s):  
Lowell T. Edgar ◽  
Steve A. Maas ◽  
James E. Guilkey ◽  
Jeffrey A. Weiss
Keyword(s):  
Type I Collagen ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Element Model ◽  
Fibrillar Structure ◽  
Type I ◽  
Major Pathway ◽  
Vessel Growth ◽  
Discrete Finite Element

Recent developments in tissue engineering have created demand for the ability to create microvascular networks with specific topologies in vitro. During angiogenesis, sprouting endothelial cells apply traction forces and migrate along components of the extracellular matrix (ECM), resulting in neovessel elongation [1]. The fibrillar structure of the ECM serves as the major pathway for mechanotransduction between contact-dependent cells. Using a three-dimensional (3D) organ culture model of microvessel fragments within a type-I collagen gel, we have shown that subjecting the culture to different boundary conditions during angiogenesis can lead to drastically different vascular topologies [2]. Fragments cultured in a rectangular gel that were free to contract grew into a randomly oriented network [3, 4]. When the long-axis of the gel was constrained as to prevent contraction, microvessels and collagen fibers were found aligned along the constrained axis (Fig. 1) [4].

scholarly journals Reciprocal Modulation of Matrix Metalloproteinase-13 and Type I Collagen Genes in Rat Hepatic Stellate Cells

2003 ◽  
Vol 162 (6) ◽  
pp. 1771-1780 ◽  
Author(s):  
Benjamin Schaefer ◽  
Ana María Rivas-Estilla ◽  
Noemí Meraz-Cruz ◽  
Miguel Arturo Reyes-Romero ◽  
Zamira H. Hernández-Nazara ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Hepatic Stellate Cells ◽  
Type I Collagen ◽  
Stellate Cells ◽  
Type I ◽  
Matrix Metalloproteinase 13 ◽  
Collagen Genes

Hematopoietic Origin of Hepatic Stellate Cell.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1679-1679
Author(s):  
Eri Miyata ◽  
Masahiro Masuya ◽  
Fumihiko Ishikawa ◽  
Shuro Yoshida ◽  
Keizo Kato ◽  
...  
Keyword(s):  
Stem Cells ◽  
Liver Injury ◽  
Hematopoietic Stem Cells ◽  
Hepatic Stellate Cells ◽  
Type I Collagen ◽  
Stellate Cells ◽  
Gradual Transition ◽  
Type I ◽  
Chimeric Mice ◽  
Hematopoietic Stem

Abstract Hepatic stellate cells are believed to play a key role in the development of liver fibrosis. They undergo a gradual transition from a quiescent, fat-storing phenotype to an activated myofibroblast-like phenotype and then produce high amount of extracellular matrix such as collagen by liver injury. They express mesenchymal markers such as vimentin and desmin, or neural/neuroectodermal markers such as glial fibrillary acidic protein (GFAP). Based on the characteristic phenotype, the embryonic origin of stellate cells is thought to be the septum transversum mesenchyme or neural crest. However, their origin in the adult liver is still unknown. Recently, several studies have reported that crude bone marrow (BM) cells can give rise to hepatic stellate cells. However, since adult BM cells are thought to contain hematopoietic stem cells and mesenchymal stem cells, it is important to clarify which type of stem cells is the true source of hepatic stellate cells. We hypothesized that hepatic stellate cells are derived from hematopoietic stem cells. To test this hypothesis, we generated chimeric mice by transplantation of singe enhanced green fluorescent protein (EGFP)-marked hematopoietic stem cells (Lin− Sca-1+ c-kit+ CD34− cells) into lethally irradiated nontransgenic mice and examined the histology of liver tissues obtained from chimeric mice with carbon tetrahydrochloride (CCl4)-induced injury. Following 12 weeks treatment of CCl4, hepatic nodules and bridging fibrosis developed in all livers. We detected EGFP+ cells in the liver and some of them contained intracytoplasmic lipid droplets, which were proved by oil red O staining. Immunohistochemical analysis demonstrated that 60% of EGFP+ cells were negative for leukocyte common antigen (CD45); however, they expressed vimentin, GFAP and ADAMTS-13, which is a circulating zinc metalloproteinase synthesized in hepatic stellate cells. Moreover, nonparenchymal cell populations were isolated from the livers of chimeric mice with CCl4 treatment and were incubated on noncoated glass slides for 3 days. EGFP+ cells were also positive for type I collagen. These phenotypes are consistent with those of hepatic stellate cells. Our findings suggest that hematopoietic stem cells contribute to the generation of hepatic stellate cells upon liver injury.

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