PMID- 34915763
OWN - NLM
STAT- MEDLINE
DCOM- 20220215
LR  - 20230202
IS  - 1551-5044 (Electronic)
IS  - 0022-1554 (Print)
IS  - 0022-1554 (Linking)
VI  - 70
IP  - 2
DP  - 2022 Feb
TI  - Evaluation of PGP 9.5, NGFR, TGFbeta1, FGFR1, MMP-2, AT2R2, SHH, and TUNEL in 
      Primary Obstructive Megaureter Tissue.
PG  - 139-149
LID - 10.1369/00221554211063515 [doi]
AB  - Primary obstructive megaureter (POM) morphogenesis is not fully known. The aim of 
      the study was to evaluate the appearance of different factors that might take 
      part in the pathogenesis of POM. Megaureter tissues of 14 children were stained 
      with hematoxylin and eosin as well as with immunohistochemistry for protein gene 
      product 9.5, nerve growth factor receptor, transforming growth factor beta 1 
      (TGFbeta1), fibroblast growth factor receptor 1 (FGFR1), matrix metalloproteinase 2 
      (MMP-2), angiotensin 2 receptor type 2, and sonic hedgehog (SHH) protein. 
      Apoptosis was detected by terminal dUTP nick-end labeling reaction. POM tissues 
      revealed transitional epithelium with scattered vacuolization, submucosa with 
      inflammatory cells, and focally vacuolized and chaotically organized muscle 
      layers. Apoptosis, appearance of MMP-2, FGFR1, and SHH prevailed, but TGFbeta1 
      positive cell number was lower in patients. Correlation between MMP-2 in 
      epithelium and endothelium, FGFR1 and MMP-2 in epithelium, and TGFbeta1 in 
      epithelium and connective tissue in patients was detected. POM morphopathogenesis 
      involves an apoptotic cell death of epithelium and smooth muscle as well as 
      tissue degradation in epithelium and connective tissue of the ureter wall. The 
      decrease of tissue growth through diminished TGFbeta1 expression and stimulation of 
      FGFR1 and MMP-2 suggests a disbalance of tissue remodelation in the megaureter 
      wall.
FAU - Junga, Anna
AU  - Junga A
AUID- ORCID: 0000-0002-6650-483X
AD  - Institute of Anatomy and Anthropology, Riga Stradins University, Riga, Latvia.
FAU - Sinicins, Ivo
AU  - Sinicins I
AD  - Institute of Anatomy and Anthropology, Riga Stradins University, Riga, Latvia.
FAU - Petersons, Aigars
AU  - Petersons A
AD  - Department of Children Surgery, Riga Stradins University, Riga, Latvia.
FAU - Pilmane, Mara
AU  - Pilmane M
AD  - Institute of Anatomy and Anthropology, Riga Stradins University, Riga, Latvia.
LA  - eng
PT  - Journal Article
DEP - 20211217
PL  - United States
TA  - J Histochem Cytochem
JT  - The journal of histochemistry and cytochemistry : official journal of the 
      Histochemistry Society
JID - 9815334
RN  - 0 (Hedgehog Proteins)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (LIM Domain Proteins)
RN  - 0 (NGFR protein, human)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 0 (SHH protein, human)
RN  - 0 (TGFB1I1 protein, human)
RN  - 0 (UCHL1 protein, human)
RN  - EC 2.7.10.1 (FGFR1 protein, human)
RN  - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
RN  - EC 3.4.19.12 (Ubiquitin Thiolesterase)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
SB  - IM
MH  - Adolescent
MH  - Child
MH  - Child, Preschool
MH  - Female
MH  - Hedgehog Proteins/genetics/metabolism
MH  - Humans
MH  - *In Situ Nick-End Labeling
MH  - Infant
MH  - Intracellular Signaling Peptides and Proteins/genetics/metabolism
MH  - LIM Domain Proteins/genetics/metabolism
MH  - Male
MH  - Matrix Metalloproteinase 2/genetics/metabolism
MH  - Nerve Tissue Proteins/genetics/metabolism
MH  - Receptor, Angiotensin, Type 2/genetics/metabolism
MH  - Receptor, Fibroblast Growth Factor, Type 1/genetics/metabolism
MH  - Receptors, Nerve Growth Factor/genetics/metabolism
MH  - Ubiquitin Thiolesterase/genetics/metabolism
MH  - Ureteral Obstruction/*genetics/metabolism
PMC - PMC8777373
OTO - NOTNLM
OT  - atrophy
OT  - development
OT  - growth factors
OT  - innervation
COIS- Competing Interests: The author(s) declared no potential conflicts of interest 
      with respect to the research, authorship, and/or publication of this article.
EDAT- 2021/12/18 06:00
MHDA- 2022/02/16 06:00
PMCR- 2023/02/01
CRDT- 2021/12/17 05:33
PHST- 2021/12/18 06:00 [pubmed]
PHST- 2022/02/16 06:00 [medline]
PHST- 2021/12/17 05:33 [entrez]
PHST- 2023/02/01 00:00 [pmc-release]
AID - 10.1369_00221554211063515 [pii]
AID - 10.1369/00221554211063515 [doi]
PST - ppublish
SO  - J Histochem Cytochem. 2022 Feb;70(2):139-149. doi: 10.1369/00221554211063515. 
      Epub 2021 Dec 17.