Collagen synthesis by mesenchymal stem cells and aortic valve interstitial cells in response to mechanical stretch

Ku, Ching-Hsin; Johnson, Peter; Batten, Puspa; Sarathchandra, Padmini; Chambers, Rachel C.; Taylor, Patricia M.; Yacoub, Magdi H.; Chester, Adrian H.

doi:10.1016/j.cardiores.2006.03.022

Cited by 162 publications

(127 citation statements)

References 22 publications

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“…Cells grown in stem cell medium without AICAR were negative for ␣-SMA. All cells, regardless of treatment, expressed collagen type I, in agreement with the findings of others 38 . These results demonstrate that activation of the AMPK pathway forced some progenitor cells to mature into myofibroblasts despite their maintenance in stem cell medium.…”

Section: Rescue Of Defective Function Requires Ampk Activationsupporting

confidence: 92%

Defective Myofibroblast Formation from Mesenchymal Stem Cells in the Aging Murine Heart

Cieslik

Trial

Entman

2011

The American Journal of Pathology

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Cardiac fibroblasts are the most prevalent cell type in the heart. These cells exert a critical role in regulating normal myocardial function and in the adverse myocardial remodeling that occurs after myocardial infarction (MI). 1 Irreversible cardiomyocyte damage owing to cessation of oxygen supply during MI leads to necrosis, which stimulates inflammatory reactions that trigger reparative pathways and activate cells to form a scar. Cytokines released by inflammatory infiltrating leukocytes promote endogenous mesenchymal stem cell (MSC) proliferation and migration toward the infarct site, followed by differentiation into fibroblasts that deposit scar-forming collagen. The fibroblasts mature into myofibroblasts, expressing scar-contracting ␣-smooth muscle actin (␣-SMA). 2 Resident fibroblasts also become activated and participate in this process. After several weeks, a mature scar is formed, and most of the myofibroblasts undergo apoptosis. [3][4][5] We have previously established in a model of mouse MI that, compared with young animals, aged mice demonstrate greater infarct expansion and less effective myocardial repair. 6 Defective scar formation arises from a decreased number of myofibroblasts and diminished collagen deposition in the infarct, which results in a structurally unstable scar formed by loose connective tissue. 7 Evidence indicates that multipotent cells can be generated in vitro from several adult organs including the heart. 8 Tissue-resident progenitor cells of mesenchymal origin can differentiate into myogenic, adipocytic, chondrocytic, osteoblastic, and fibroblastic lineages. 9 -11 The potential of those stem cells to differentiate decreases

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Section: Rescue Of Defective Function Requires Ampk Activationsupporting

confidence: 92%

Defective Myofibroblast Formation from Mesenchymal Stem Cells in the Aging Murine Heart

Cieslik

Trial

Entman

2011

The American Journal of Pathology

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“…For instance Ku et al (2006) and Song et al (2007) show a positive correlation, while according to Simmons (2003), even small mechanical strain reduces the proliferation rate of mesenchymal cells. For now only the later results are included in this study.…”

Section: Appendix A: Parameters Of the Tissue Differentiation Modelmentioning

confidence: 95%

Simulation of fracture healing incorporating mechanoregulation of tissue differentiation and dispersal/proliferation of cells

Andreykiv

Keulen

Prendergast

2007

Biomech Model Mechanobiol

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Modelling the course of healing of a long bone subjected to loading has been the subject of several investigations. These have succeeded in predicting the differentiation of tissues in the callus in response to a static mechanical load and the diffusion of biological factors. In this paper an approach is presented which includes both mechanoregulation of tissue differentiation and the diffusion and proliferation of cell populations (mesenchymal stem cells, fibroblasts, chondrocytes, and osteoblasts). This is achieved in a three-dimensional poroelastic finite element model which, being poroelastic, can model the effect of the frequency of dynamic loading. Given the number of parameters involved in the simulation, a parameter variation study is reported, and final parameters are selected based on comparison with an in vivo experiment. The model predicts that asymmetric loading creates an asymmetric distribution of tissues in the callus, but only for high bending moments. Furthermore the frequency of loading is predicted to have an effect. In conclusion, a numerical algorithm is presented incorporating both mechanoregulation and evolution of cell populations, and it proves capable of predicting realistic difference in bone healing in a 3D fracture callus.

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“…Collagen synthesis was assessed by measuring the uptake of [ 3 H] proline as previously described with slight modifications (Ku et al, 2006). Briefly cells were seeded into 24-well plates.…”

Section: Measurement Of Total Collagen Synthesis By [ 3 H] Proline Inmentioning

confidence: 99%

“…The major biosynthetic destination of proline is collagen and therefore the amounts of radioactive [ 3 H] proline incorporated into insoluble and soluble protein fractions provides a reliable index of total collagen synthesis (Mukherjee and Sen 1990;Ku et al, 2006). In order to determine the receptors involved in ET-1 mediated increase in collagen synthesis, the cells were preincubated with either an ET A receptor antagonist, BQ610 (1μM) or an ET B receptor antagonist, BQ788 (1μM) and subsequently treated with ET-1 for 48hrs in the presence of [ 3 H] proline.…”

Section: Et-1 Mediated Regulation Of Collagen Synthesis In Lc Cells Amentioning

confidence: 99%

Endothelin-1 mediated regulation of extracellular matrix collagens in cells of human lamina cribrosa

Rao

Krishnamoorthy

Yorio

2008

Experimental Eye Research

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Endothelin-1(ET-1), a potent vaso-active peptide, mediates extracellular matrix regulation resulting in an increase in collagen deposition in various cell types and tissues and has been proposed to play a key role in glaucoma pathology. The role of ET-1 in the regulation of extracellular matrix collagens at the level of optic nerve head is not known. In this study we have examined the role of ET-1 in extracellular matrix collagen regulation in primary cultures of human lamina cribrosa cells. Our hypothesis is that ET-1 increases remodeling of the ECM of cells of the lamina cribrosa. Such actions could contribute to the development of optic neuropathy. QPCR analysis revealed that ET-1 mediated an increase in mRNA levels of collagen type I alpha 1 and collagen type VI alpha 1 chains at all doses of ET-1 with a significant increase at 1nM and 10nM concentration in LC cells. A dose dependent increase in collagen type I and type VI protein deposition and secretion was also observed by Western blot in response to ET-1 and was significant at 10nM and 100nM concentrations of ET-1. ET-1 increased the [ 3 H] proline uptake in LC cells suggesting that ET-1 contributed to an increase in total collagen synthesis in LC cells. ET-1 -mediated increase in collagen type I, type VI and total collagen synthesis was significantly blocked by the ET A receptor antagonist, BQ610, as well as with the ET B receptor antagonist, BQ788, suggesting the involvement of both receptor subtypes in ET-1 mediated collagen synthesis in LC cells. These results suggest that ET-1 regulates extra cellular matrix-collagen synthesis in LC cells and may contribute to ECM remodeling at the level of LC of POAG subjects who have elevated plasma and aqueous humor levels of endothelin-1.

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Collagen synthesis by mesenchymal stem cells and aortic valve interstitial cells in response to mechanical stretch

Cited by 162 publications

References 22 publications

Defective Myofibroblast Formation from Mesenchymal Stem Cells in the Aging Murine Heart

Defective Myofibroblast Formation from Mesenchymal Stem Cells in the Aging Murine Heart

Simulation of fracture healing incorporating mechanoregulation of tissue differentiation and dispersal/proliferation of cells

Endothelin-1 mediated regulation of extracellular matrix collagens in cells of human lamina cribrosa

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