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The involvement of advanced glycation endproducts (AGEs) in renal injury of diabetic glomerulosclerosis: association with phenotypic change in renal cells and infiltration of immune cells.
Clin Exp Nephrol 2003; 7(3):201-9CE

Abstract

BACKGROUND

Glycation of proteins is regarded as one of the major causes of the progression of diabetic nephropathy (DN) and of the phenotypic changes in glomerular mesangial cells (MC) and the cellular infiltration that occurs in MC from DN. It thus is very important to study the interrelationships and interaction between these causes.

METHODS

The localization of advanced glycation endproducts (AGEs), cytoskeletal proteins, and immune cell infiltration was evaluated by immunohistochemical study in patients with DN.

RESULTS

N(Epsilon)-(carboxymethyl)lysine (CML), Alpha-smooth muscle actin (SMA), and low-molecular-weight caldesmon (L-CLD) were localized in the mesangial area in DN. The intensity of mesangial SMA and L-CLD expression was significantly correlated with the index of diabetic glomerulosclerosis (IDGS), while the expression of pentosidine was correlated with the IDGS and with 24-h urinary protein. Pentosidine was localized in glomerular basement membrane (GBM) only in DN and had a significant correlation with the mesangial expression of SMA and L-CLD. Pyrraline deposition on the tubular basement membrane, and the expression of SMA and L-CLD, and the infiltration of immune cells were observed in interstitial areas in DN. The intensity of L-CLD expression had a close relationship with pyrraline deposition and immune cell infiltration. The expression of SMA and L-CLD in interstitial areas was significantly correlated with the percent interstitial volume.

CONCLUSIONS

AGEs are involved in renal injury in DN, and their effect is, at least in part, exercised via phenotypic changes in intrinsic renal cells and by the infiltration of immune cells.

Authors+Show Affiliations

Department of Nephrology of Beijing Hospital, Beijing, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14586716

Citation

Mao, Yonghui, et al. "The Involvement of Advanced Glycation Endproducts (AGEs) in Renal Injury of Diabetic Glomerulosclerosis: Association With Phenotypic Change in Renal Cells and Infiltration of Immune Cells." Clinical and Experimental Nephrology, vol. 7, no. 3, 2003, pp. 201-9.
Mao Y, Ootaka T, Saito T, et al. The involvement of advanced glycation endproducts (AGEs) in renal injury of diabetic glomerulosclerosis: association with phenotypic change in renal cells and infiltration of immune cells. Clin Exp Nephrol. 2003;7(3):201-9.
Mao, Y., Ootaka, T., Saito, T., Sato, H., Sato, T., & Ito, S. (2003). The involvement of advanced glycation endproducts (AGEs) in renal injury of diabetic glomerulosclerosis: association with phenotypic change in renal cells and infiltration of immune cells. Clinical and Experimental Nephrology, 7(3), pp. 201-9.
Mao Y, et al. The Involvement of Advanced Glycation Endproducts (AGEs) in Renal Injury of Diabetic Glomerulosclerosis: Association With Phenotypic Change in Renal Cells and Infiltration of Immune Cells. Clin Exp Nephrol. 2003;7(3):201-9. PubMed PMID: 14586716.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The involvement of advanced glycation endproducts (AGEs) in renal injury of diabetic glomerulosclerosis: association with phenotypic change in renal cells and infiltration of immune cells. AU - Mao,Yonghui, AU - Ootaka,Tetsuya, AU - Saito,Takao, AU - Sato,Hiroshi, AU - Sato,Toshinobu, AU - Ito,Sadayoshi, PY - 2002/12/13/received PY - 2003/06/22/accepted PY - 2003/10/31/pubmed PY - 2003/12/16/medline PY - 2003/10/31/entrez SP - 201 EP - 9 JF - Clinical and experimental nephrology JO - Clin. Exp. Nephrol. VL - 7 IS - 3 N2 - BACKGROUND: Glycation of proteins is regarded as one of the major causes of the progression of diabetic nephropathy (DN) and of the phenotypic changes in glomerular mesangial cells (MC) and the cellular infiltration that occurs in MC from DN. It thus is very important to study the interrelationships and interaction between these causes. METHODS: The localization of advanced glycation endproducts (AGEs), cytoskeletal proteins, and immune cell infiltration was evaluated by immunohistochemical study in patients with DN. RESULTS: N(Epsilon)-(carboxymethyl)lysine (CML), Alpha-smooth muscle actin (SMA), and low-molecular-weight caldesmon (L-CLD) were localized in the mesangial area in DN. The intensity of mesangial SMA and L-CLD expression was significantly correlated with the index of diabetic glomerulosclerosis (IDGS), while the expression of pentosidine was correlated with the IDGS and with 24-h urinary protein. Pentosidine was localized in glomerular basement membrane (GBM) only in DN and had a significant correlation with the mesangial expression of SMA and L-CLD. Pyrraline deposition on the tubular basement membrane, and the expression of SMA and L-CLD, and the infiltration of immune cells were observed in interstitial areas in DN. The intensity of L-CLD expression had a close relationship with pyrraline deposition and immune cell infiltration. The expression of SMA and L-CLD in interstitial areas was significantly correlated with the percent interstitial volume. CONCLUSIONS: AGEs are involved in renal injury in DN, and their effect is, at least in part, exercised via phenotypic changes in intrinsic renal cells and by the infiltration of immune cells. SN - 1342-1751 UR - https://www.unboundmedicine.com/medline/citation/14586716/The_involvement_of_advanced_glycation_endproducts__AGEs__in_renal_injury_of_diabetic_glomerulosclerosis:_association_with_phenotypic_change_in_renal_cells_and_infiltration_of_immune_cells_ L2 - https://dx.doi.org/10.1007/s10157-003-0245-z DB - PRIME DP - Unbound Medicine ER -