PMID- 23061002
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121015
LR  - 20211021
IS  - 2005-6745 (Electronic)
IS  - 2005-6737 (Print)
IS  - 2005-6737 (Linking)
VI  - 53
IP  - 9
DP  - 2012 Sep
TI  - Differential expression of nerve injury-induced protein 1 (ninjurin 1) in in vivo 
      and in vitro models for diabetic erectile dysfunction.
PG  - 636-42
LID - 10.4111/kju.2012.53.9.636 [doi]
AB  - PURPOSE: Endothelial dysfunction and peripheral neuropathy are important 
      mechanisms responsible for diabetes-induced erectile dysfunction (ED). Nerve 
      injury-induced protein 1 (Ninjurin 1) is known to be related to neuroinflammatory 
      processes and is also reported to induce vascular regression during the 
      developmental period. In the present study, we determined the differential 
      expression of Ninjurin 1 in penile tissue of streptozotocin (STZ)-induced 
      diabetic mice with ED. MATERIALS AND METHODS: Diabetes was induced in 8-week-old 
      C57BL/6J mice by intraperitoneal injections of STZ (50 mg/kg for 5 days). Eight 
      weeks later, erectile function was measured by electrical stimulation of the 
      cavernous nerve (n=6 per group). The penis was then harvested for 
      immunohistochemical analysis and Western blot analysis for Ninjurin 1 (n=4 per 
      group). We also determined Ninjurin 1 expression in primary cultured mouse 
      cavernous endothelial cells (MCECs) incubated under the following conditions: 
      normal glucose condition (5 mM), high-glucose condition (30 mM), and high-glucose 
      condition (30 mM)+insulin (1 nM). RESULTS: The expression of Ninjurin 1 protein 
      was significantly higher in both cavernous endothelial cells and the dorsal nerve 
      bundle of diabetic mice than in those of controls. In the in vitro study in 
      MCECs, Ninjurin 1 expression was also significantly increased by the high-glucose 
      condition and was returned to baseline levels by treatment with insulin. 
      CONCLUSIONS: Regarding the role of Ninjurin 1 in neuropathy and vascular 
      regression, it would be interesting to examine the effects of inhibition of 
      Ninjurin 1 on erectile function in animal models of ED with a vascular or 
      neurogenic cause.
FAU - Kim, Do Kyung
AU  - Kim DK
AD  - Department of Urology, National Research Center for Sexual Medicine, Inha 
      University School of Medicine, Incheon, Korea.
FAU - Yin, Guo Nan
AU  - Yin GN
FAU - Ryu, Ji Kan
AU  - Ryu JK
FAU - Suh, Jun Kyu
AU  - Suh JK
LA  - eng
PT  - Journal Article
DEP - 20120919
PL  - Korea (South)
TA  - Korean J Urol
JT  - Korean journal of urology
JID - 101499376
PMC - PMC3460007
OTO - NOTNLM
OT  - Diabetes mellitus
OT  - Endothelium
OT  - Erectile dysfunction
OT  - Nerve
OT  - Ninj1
COIS- The authors have nothing to disclose.
EDAT- 2012/10/13 06:00
MHDA- 2012/10/13 06:01
PMCR- 2012/09/01
CRDT- 2012/10/13 06:00
PHST- 2012/05/22 00:00 [received]
PHST- 2012/08/08 00:00 [accepted]
PHST- 2012/10/13 06:00 [entrez]
PHST- 2012/10/13 06:00 [pubmed]
PHST- 2012/10/13 06:01 [medline]
PHST- 2012/09/01 00:00 [pmc-release]
AID - 10.4111/kju.2012.53.9.636 [doi]
PST - ppublish
SO  - Korean J Urol. 2012 Sep;53(9):636-42. doi: 10.4111/kju.2012.53.9.636. Epub 2012 
      Sep 19.