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Modified citrus pectin reduces galectin-3 expression and disease severity in experimental acute kidney injury.
PLoS One. 2011 Apr 08; 6(4):e18683.Plos

Abstract

Galectin-3 is a β-galactoside binding lectin with roles in diverse processes including proliferation, apoptosis, inflammation and fibrosis which are dependent on different domains of the molecule and subcellular distribution. Although galectin-3 is known to be upregulated in acute kidney injury, the relative importance of its different domains and functions are poorly understood in the underlying pathogenesis. Therefore we experimentally modulated galectin-3 in folic acid (FA)-induced acute kidney injury utilising modified citrus pectin (MCP), a derivative of pectin which can bind to the galectin-3 carbohydrate recognition domain thereby predominantly antagonising functions linked to this role. Mice were pre-treated with normal or 1% MCP-supplemented drinking water one week before FA injection. During the initial injury phase, all FA-treated mice lost weight whilst their kidneys enlarged secondary to the renal insult; these gross changes were significantly lessened in the MCP group but this was not associated with significant changes in galectin-3 expression. At a histological level, MCP clearly reduced renal cell proliferation but did not affect apoptosis. Later, during the recovery phase at two weeks, MCP-treated mice demonstrated reduced galectin-3 in association with decreased renal fibrosis, macrophages, pro-inflammatory cytokine expression and apoptosis. Other renal galectins, galectin-1 and -9, were unchanged. Our data indicates that MCP is protective in experimental nephropathy with modulation of early proliferation and later galectin-3 expression, apoptosis and fibrosis. This raises the possibility that MCP may be a novel strategy to reduce renal injury in the long term, perhaps via carbohydrate binding-related functions of galectin-3.

Authors+Show Affiliations

Nephro-Urology Unit, UCL Institute of Child Health, London, United Kingdom.No 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

21494626

Citation

Kolatsi-Joannou, Maria, et al. "Modified Citrus Pectin Reduces Galectin-3 Expression and Disease Severity in Experimental Acute Kidney Injury." PloS One, vol. 6, no. 4, 2011, pp. e18683.
Kolatsi-Joannou M, Price KL, Winyard PJ, et al. Modified citrus pectin reduces galectin-3 expression and disease severity in experimental acute kidney injury. PLoS One. 2011;6(4):e18683.
Kolatsi-Joannou, M., Price, K. L., Winyard, P. J., & Long, D. A. (2011). Modified citrus pectin reduces galectin-3 expression and disease severity in experimental acute kidney injury. PloS One, 6(4), e18683. https://doi.org/10.1371/journal.pone.0018683
Kolatsi-Joannou M, et al. Modified Citrus Pectin Reduces Galectin-3 Expression and Disease Severity in Experimental Acute Kidney Injury. PLoS One. 2011 Apr 8;6(4):e18683. PubMed PMID: 21494626.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modified citrus pectin reduces galectin-3 expression and disease severity in experimental acute kidney injury. AU - Kolatsi-Joannou,Maria, AU - Price,Karen L, AU - Winyard,Paul J, AU - Long,David A, Y1 - 2011/04/08/ PY - 2010/11/12/received PY - 2011/03/10/accepted PY - 2011/4/16/entrez PY - 2011/4/16/pubmed PY - 2011/8/17/medline SP - e18683 EP - e18683 JF - PloS one JO - PLoS One VL - 6 IS - 4 N2 - Galectin-3 is a β-galactoside binding lectin with roles in diverse processes including proliferation, apoptosis, inflammation and fibrosis which are dependent on different domains of the molecule and subcellular distribution. Although galectin-3 is known to be upregulated in acute kidney injury, the relative importance of its different domains and functions are poorly understood in the underlying pathogenesis. Therefore we experimentally modulated galectin-3 in folic acid (FA)-induced acute kidney injury utilising modified citrus pectin (MCP), a derivative of pectin which can bind to the galectin-3 carbohydrate recognition domain thereby predominantly antagonising functions linked to this role. Mice were pre-treated with normal or 1% MCP-supplemented drinking water one week before FA injection. During the initial injury phase, all FA-treated mice lost weight whilst their kidneys enlarged secondary to the renal insult; these gross changes were significantly lessened in the MCP group but this was not associated with significant changes in galectin-3 expression. At a histological level, MCP clearly reduced renal cell proliferation but did not affect apoptosis. Later, during the recovery phase at two weeks, MCP-treated mice demonstrated reduced galectin-3 in association with decreased renal fibrosis, macrophages, pro-inflammatory cytokine expression and apoptosis. Other renal galectins, galectin-1 and -9, were unchanged. Our data indicates that MCP is protective in experimental nephropathy with modulation of early proliferation and later galectin-3 expression, apoptosis and fibrosis. This raises the possibility that MCP may be a novel strategy to reduce renal injury in the long term, perhaps via carbohydrate binding-related functions of galectin-3. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/21494626/Modified_citrus_pectin_reduces_galectin_3_expression_and_disease_severity_in_experimental_acute_kidney_injury_ L2 - https://dx.plos.org/10.1371/journal.pone.0018683 DB - PRIME DP - Unbound Medicine ER -