The role of syndecan-1 in kidney regeneration

Seppenwoolde, D.W. (2012) The role of syndecan-1 in kidney regeneration. Bachelor's Thesis, Biology.

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Abstract

Losing kidney function is dangerous and lead to chronic renal failure. In chronic renal failure there is interstitial fibrosis (IF) and many nephrons are destroyed by tubular atrophy (TA). An ideal solution for chronic renal failure would be slowing down the disease and stimulating kidney regeneration. Kidney regeneration can be executed by kidney stem cells, bone marrow stem cells and intrinsic (epithelial) kidney cells of which the last seem to be the most important. Recent investigations showed that proteoglycans (PGs) might influence the regenerative process of the kidney. This thesis focuses on syndecan-1 which is a cell surface trans membrane PG of the heparan sulfate proteoglycans (HSPGs) family. In adult tissues, syndecan-1 is predominantly expressed by both simple and stratified epithelial cells and plasma cells. Sydecan-1 carry out its functions by serving as a co-receptor for many different receptors. Investigations showed that syndecan-1 (via the heparan sulfate side chains) might be capable of protecting and regenerating the damaged cells and therefore inducing tubule repair after injury. Syndecan-1 expression is induced by TGF- β and EGF and reduced by TNF-α and IL-1β. Syndecan-1 can also be shed from the cell surface by MMP-7, MMP-9, MMP-14 and ADAM17, resulting in soluble syndecan-1 (sSynd-1). Shedding can rapidly reduce the syndecan-1 expression on the cell surface which leads to less responsive cells. sSynd-1 can function in an autocrine or paracrine manner by binding growth factors and cytokines and then binding to the corresponding receptor. sSynd-1 may inhibit cell proliferation during wound repair and therefore can inhibit epithelial wound healing. To stimulate regeneration after injury syndecan-1 expression should be stimulated and shedding should be avoided. Syndecan-1 can be stimulated by all-trans retinoic acid (ATRA) or n-3 polyunsaturated fatty acids (n-3 PUFA) diet. Shedding can be avoided by the antioxidant enzyme extracellular superoxide dismutase (EC-SOD) or by the tissue inhibitor of metalloproteinase-3 (TIMP3). Syndecan-1 can be a novel therapeutic target in treatment of chronic renal failure.

Item Type:	Thesis (Bachelor's Thesis)
Degree programme:	Biology
Thesis type:	Bachelor's Thesis
Language:	English
Date Deposited:	15 Feb 2018 07:50
Last Modified:	15 Feb 2018 07:50
URI:	https://fse.studenttheses.ub.rug.nl/id/eprint/10374

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