Laminin alterations after in vitro nonenzymatic glycosylation - PubMed (original) (raw)
Laminin alterations after in vitro nonenzymatic glycosylation
A S Charonis et al. Diabetes. 1990 Jul.
Abstract
Laminin, a basement membrane protein derived from the matrix of the Engelbreth-Holm-Swarm murine tumor, was nonenzymatically glycosylated in vitro in the presence of increasing glucose concentrations. The amount of glucose incorporated per laminin molecule was shown to be proportional to the molarity of glucose used. Nonenzymatic glycosylation resulted in formation of cross-links and alterations of the cruciform shape of laminin molecules; these alterations were dramatic when high concentrations of glucose were used. One of the functions of laminin, the process of self-assembly, was shown to be impaired after in vitro nonenzymatic glycosylation. Glucose incorporation resulted in a dramatic decrease of long-to-long laminin dimers, which normally form during the initial steps of assembly. Furthermore, nonenzymatic glycosylation of laminin reduced its ability to self-associate into complexes larger than dimers, as judged by turbidimetry. The observed decrease of maximal turbidity was proportional to the degree of nonenzymatic glycosylation. Aminoguanidine, which has been suggested to inhibit cross-link formation, was shown to restore to a large extent the shape of laminin, the percentage of long-to-long arm dimers, and the maximal turbidity when included in the mixtures of laminin and glucose. These data suggest that structural and functional alterations of laminin may be primarily due to formation of cross-links. Such modifications of laminin (along with our basement membrane components) may contribute to the morphological and physiological changes observed in basement membranes under diabetic conditions.
Similar articles
- Molecular mechanisms in basement membrane complications of diabetes. Alterations in heparin, laminin, and type IV collagen association.
Tarsio JF, Reger LA, Furcht LT. Tarsio JF, et al. Diabetes. 1988 May;37(5):532-9. doi: 10.2337/diab.37.5.532. Diabetes. 1988. PMID: 3360214 - Altered proliferation of retinal microvascular cells on glycated matrix.
Kalfa TA, Gerritsen ME, Carlson EC, Binstock AJ, Tsilibary EC. Kalfa TA, et al. Invest Ophthalmol Vis Sci. 1995 Nov;36(12):2358-67. Invest Ophthalmol Vis Sci. 1995. PMID: 7591625 - Effects of nonenzymatic glycosylation of mesangial matrix on proliferation of mesangial cells.
Crowley ST, Brownlee M, Edelstein D, Satriano JA, Mori T, Singhal PC, Schlondorff DO. Crowley ST, et al. Diabetes. 1991 May;40(5):540-7. doi: 10.2337/diab.40.5.540. Diabetes. 1991. PMID: 1708734 - Structural and functional changes of laminin and type IV collagen after nonenzymatic glycation.
Charonis AS, Tsilbary EC. Charonis AS, et al. Diabetes. 1992 Oct;41 Suppl 2:49-51. doi: 10.2337/diab.41.2.s49. Diabetes. 1992. PMID: 1526336 Review. - Advanced nonenzymatic glycation endproducts (AGE): their relevance to aging and the pathogenesis of late diabetic complications.
Sensi M, Pricci F, Andreani D, Di Mario U. Sensi M, et al. Diabetes Res. 1991 Jan;16(1):1-9. Diabetes Res. 1991. PMID: 1818791 Review.
Cited by
- Role of advanced glycation end products in mobility and considerations in possible dietary and nutritional intervention strategies.
Chen JH, Lin X, Bu C, Zhang X. Chen JH, et al. Nutr Metab (Lond). 2018 Oct 10;15:72. doi: 10.1186/s12986-018-0306-7. eCollection 2018. Nutr Metab (Lond). 2018. PMID: 30337945 Free PMC article. Review. - Glycation Damage: A Possible Hub for Major Pathophysiological Disorders and Aging.
Fournet M, Bonté F, Desmoulière A. Fournet M, et al. Aging Dis. 2018 Oct 1;9(5):880-900. doi: 10.14336/AD.2017.1121. eCollection 2018 Oct. Aging Dis. 2018. PMID: 30271665 Free PMC article. Review. - Icodextrin and peritoneal dialysis: advantages and new applications.
Dousdampanis P, Musso CG, Trigka K. Dousdampanis P, et al. Int Urol Nephrol. 2018 Mar;50(3):495-500. doi: 10.1007/s11255-017-1647-2. Epub 2017 Jul 3. Int Urol Nephrol. 2018. PMID: 28674854 Review. - Diabetic kidney disease: a role for advanced glycation end-product receptor 1 (AGE-R1)?
Zhuang A, Forbes JM. Zhuang A, et al. Glycoconj J. 2016 Aug;33(4):645-52. doi: 10.1007/s10719-016-9693-z. Epub 2016 Jun 6. Glycoconj J. 2016. PMID: 27270766 Review. - Glycosaminoglycan remodeling during diabetes and the role of dietary factors in their modulation.
Gowd V, Gurukar A, Chilkunda ND. Gowd V, et al. World J Diabetes. 2016 Feb 25;7(4):67-73. doi: 10.4239/wjd.v7.i4.67. World J Diabetes. 2016. PMID: 26962410 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources