PMID- 30455396
OWN - NLM
STAT- MEDLINE
DCOM- 20190722
LR  - 20211204
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 38
IP  - 6
DP  - 2018 Dec 21
TI  - Galectin 3 inhibition attenuates renal injury progression in cisplatin-induced 
      nephrotoxicity.
LID - BSR20181803 [pii]
LID - 10.1042/BSR20181803 [doi]
AB  - Nephrotoxicity is a major toxic effect in chemotherapy, which constitutes up to 
      60% of hospitalized acute kidney injury (AKI). Very few treatment options exist 
      to slow the transition from AKI to subsequent chronic kidney diseases (CKD). 
      Here, we demonstrate that galectin-3 (Gal-3), a beta-galactoside binding lectin that 
      plays an important role in kidney fibrosis and renal failure, is one of the key 
      factors for renal injury progression. Ectopic overexpression of Gal-3 
      significantly decreased the viability of HEK293, simultaneously inducing of cell 
      cycle arrest and apoptosis. However, inhibition of Gal-3, mediated by modified 
      citrus pectin (MCP), predominantly antagonized the pro-apoptotic effects. Mice 
      were pre-treated with normal or 1% MCP-supplemented drinking water 1 week before 
      cisplatin injection. Analyses of serum creatinine and renal tissue damage 
      indicated that MCP-treated mice demonstrated increased renal function and 
      attenuated renal fibrosis after cisplatin-induced injury. MCP-treated mice also 
      demonstrated decreased renal fibrosis and apoptosis, as revealed by masson 
      trichrome staining and Western blot analysis of cleaved caspase-3. Additionally, 
      the protective role of Gal-3 inhibition in the kidney injury was shown to be 
      mediated by protein kinase C alpha (PKC-alpha), which promoted cell apoptosis and 
      collagen I synthesis in HEK293 cells. These results demonstrated the potential 
      Gal-3 and PKC-alpha as therapeutic targets for the treatment of AKI and CKD.
CI  - (c) 2018 The Author(s).
FAU - Li, Hong-Yan
AU  - Li HY
AUID- ORCID: 0000-0002-3307-4028
AD  - Division of Nephrology, Huadu District People's Hospital of Guangzhou, Southern 
      Medical University, Guangzhou 510800, P.R. China (lihy0726@126.com 
      (fengjx9101@126.com.
FAU - Yang, Shen
AU  - Yang S
AD  - Division of Nephrology, Huadu District People's Hospital of Guangzhou, Southern 
      Medical University, Guangzhou 510800, P.R. China.
FAU - Li, Jing-Chun
AU  - Li JC
AD  - Division of Nephrology, Huadu District People's Hospital of Guangzhou, Southern 
      Medical University, Guangzhou 510800, P.R. China.
FAU - Feng, Jian-Xun
AU  - Feng JX
AD  - Division of Nephrology, Xuhui District Centeral Hospital of Shanghai, Shanghai, 
      P.R. China (lihy0726@126.com (fengjx9101@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181218
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (Blood Proteins)
RN  - 0 (Galectin 3)
RN  - 0 (Galectins)
RN  - 0 (LGALS3 protein, human)
RN  - 47EQO8LE7H (citrus pectin)
RN  - 89NA02M4RX (Pectins)
RN  - AYI8EX34EU (Creatinine)
RN  - EC 2.7.11.13 (Protein Kinase C-alpha)
RN  - EC 3.4.22.- (Caspase 3)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Acute Kidney Injury/blood/chemically induced/*genetics/pathology
MH  - Animals
MH  - Apoptosis/genetics
MH  - Blood Proteins
MH  - Caspase 3/genetics
MH  - Cisplatin/administration & dosage/*adverse effects
MH  - Creatinine/blood
MH  - Disease Models, Animal
MH  - Fibrosis/blood/chemically induced/*genetics/pathology
MH  - Galectin 3/antagonists & inhibitors/*genetics
MH  - Galectins
MH  - Gene Expression Regulation
MH  - Humans
MH  - Kidney/drug effects/metabolism/pathology
MH  - Mice
MH  - Neoplasms/complications/drug therapy
MH  - Pectins/genetics
MH  - Protein Kinase C-alpha/*genetics
MH  - Renal Insufficiency, Chronic/blood/genetics/pathology
PMC - PMC6435560
OTO - NOTNLM
OT  - acute kidney injury
OT  - apoptosis
OT  - galectin-3
OT  - modified citrus pectin
OT  - renal fibrosis
COIS- The authors declare that there are no competing interests associated with the 
      manuscript.
EDAT- 2018/11/21 06:00
MHDA- 2019/07/23 06:00
PMCR- 2018/12/18
CRDT- 2018/11/21 06:00
PHST- 2018/10/08 00:00 [received]
PHST- 2018/11/12 00:00 [revised]
PHST- 2018/11/15 00:00 [accepted]
PHST- 2018/11/21 06:00 [pubmed]
PHST- 2019/07/23 06:00 [medline]
PHST- 2018/11/21 06:00 [entrez]
PHST- 2018/12/18 00:00 [pmc-release]
AID - BSR20181803 [pii]
AID - 10.1042/BSR20181803 [doi]
PST - epublish
SO  - Biosci Rep. 2018 Dec 18;38(6):BSR20181803. doi: 10.1042/BSR20181803. Print 2018 
      Dec 21.