PMID- 23601763
OWN - NLM
STAT- MEDLINE
DCOM- 20140115
LR  - 20220408
IS  - 1532-2777 (Electronic)
IS  - 0306-9877 (Linking)
VI  - 81
IP  - 1
DP  - 2013 Jul
TI  - Epithelial-mesenchymal transition of renal tubules: divergent processes of 
      repairing in acute or chronic injury?
PG  - 73-5
LID - S0306-9877(13)00138-2 [pii]
LID - 10.1016/j.mehy.2013.03.020 [doi]
AB  - Epithelial-mesenchymal transition (EMT) of tubular epithelial cells (TECs) is 
      commonly considered as the major mechanism leading to renal fibrosis in chronic 
      kidney diseases (CKD) injury. We raise the hypothesis that EMT in adult kidney 
      may be an event of "atavistic" phenotypic transition, which mimics but reverses 
      the genetic and cellular processes of development of renal tubules. Transformed 
      TECs may be regarded as induced mesenchymal stem-like cells, representing a 
      cellular self-adaptation when in acute or chronic injury. The reasons are as 
      follows: (1) Embryonic gene WT1 and Pax2, which govern tubule development, have 
      been found to re-express during tubular EMT when facing injury. (2) The common 
      factors that induce EMT in vitro, like IL-1, angiotension II and hypoxia could 
      also promote WT1 and/or Pax2 re-expression. (3) Expression of WT1 and Pax2 are 
      found to be associated with progenitor cells. (4) Beside embryonic gene WT1 and 
      Pax2, we also found that some stem cell markers like CD133 were expressed during 
      EMT process. (5) The process of EMT is not only take place in chronic kidney 
      injury (CKD), but also in acute kidney injury (AKI) as well. (6) The phenotype 
      transition of TECs and genetic event during AKI are entirely consistent with what 
      happened in CKD, but the outcome is completely different. Thus, we thought 
      tubular injury of CKD and AKI may share a common initiative repair mechanism: 
      tubular EMT, that is TECs are transformed into induced mesenchymal stem-like 
      cells, and then interpret the injurious signal differently in acute versus 
      chronic conditions, so as to possess a divergent fates, tubular regeneration or 
      fibrosis formation, depending on a different microenvironment or the duration of 
      the injury. In this sense, tubular EMT could be purposefully orientated into a 
      constructively pathway that repair kidney injury via tubular regeneration, matrix 
      remodeling and tissue structure and function restoration.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Jiang, Y S
AU  - Jiang YS
AD  - Department of Laboratory Medicine, The First Affiliated Hospital of Sun Yat-sen 
      University, 58 2nd Zhongshan Road, Guangzhou, Guangdong 510080, China.
FAU - Jiang, T
AU  - Jiang T
FAU - Huang, B
AU  - Huang B
FAU - Chen, P S
AU  - Chen PS
FAU - Ouyang, J
AU  - Ouyang J
LA  - eng
PT  - Journal Article
DEP - 20130416
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (AC133 Antigen)
RN  - 0 (Antigens, CD)
RN  - 0 (Glycoproteins)
RN  - 0 (PAX2 Transcription Factor)
RN  - 0 (PAX2 protein, human)
RN  - 0 (PROM1 protein, human)
RN  - 0 (Peptides)
SB  - IM
MH  - AC133 Antigen
MH  - Antigens, CD/immunology
MH  - *Epithelial-Mesenchymal Transition
MH  - Genes, Wilms Tumor
MH  - Glycoproteins/immunology
MH  - Humans
MH  - Kidney Failure, Chronic/genetics/*pathology
MH  - Kidney Tubules/*pathology
MH  - PAX2 Transcription Factor/genetics
MH  - Peptides/immunology
EDAT- 2013/04/23 06:00
MHDA- 2014/01/16 06:00
CRDT- 2013/04/23 06:00
PHST- 2012/07/24 00:00 [received]
PHST- 2013/03/09 00:00 [accepted]
PHST- 2013/04/23 06:00 [entrez]
PHST- 2013/04/23 06:00 [pubmed]
PHST- 2014/01/16 06:00 [medline]
AID - S0306-9877(13)00138-2 [pii]
AID - 10.1016/j.mehy.2013.03.020 [doi]
PST - ppublish
SO  - Med Hypotheses. 2013 Jul;81(1):73-5. doi: 10.1016/j.mehy.2013.03.020. Epub 2013 
      Apr 16.