Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P04179 (
MnSOD
)
2,777
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Pancreatic islets are particularly vulnerable in the initial days after transplantation when multiple factors converge to damage the islet graft. The aim of this study was to investigate the expression profile of genes involved in damage and protection of beta-cells in the initial days after syngeneic islet transplantation. We studied the expression of a set of selected genes involved in apoptosis (Bcl2, Bclx(L), Bax, Bad, Bid, and
CHOP
), cytokine defense, (SOCS-1 and SOCS-3), or free radical protection (Hmox1, Cu/Zn-SOD,
Mn-SOD
, and Hsp70). Because hyperglycemia has deleterious effects on islet transplantation outcome, we studied its effect on the expression of these genes. Five hundred islets were syngeneically transplanted under the kidney capsule of normoglycemic or streptozotocin-induced diabetic Lewis rats. Gene expression was analyzed by quantitative real-time RT-PCR in grafts 1, 3, and 7 days after transplantation, and in freshly isolated islets. The expression of proapoptotic genes Bid and
CHOP
, as well as protective genes Bclx(L), Socs1, Socs3, Hmox1, and MnSod, was maximally increased 1 day after transplantation, and in most cases it remained increased 7 days later, indicating the presence of a protective response against cell damage. In contrast, the expression of Bcl2, Bax, Bad, Cu/ZnSod, and Hsp70 genes did not change. Hyperglycemia did not modify the expression of most studied genes. However, MnSod and Ins2 expression was increased and reduced, respectively, on day 7 after transplantation to diabetic recipients, suggesting that hyperglycemia increased oxidative stress and deteriorated beta-cell function in transplanted islets.
...
PMID:Islet graft response to transplantation injury includes upregulation of protective as well as apoptotic genes. 1917 39
The phenotypes of
calbindin-D9k
- (
CaBP-9k
-) knockout (KO),
calbindin
-
D28k
- (
CaBP-28k
-) KO, and
CaBP-9k/28k
-KO mice are similar to those of wild-type (WT) mice due to the compensatory action of other calcium transport proteins. In this study, we investigated the expression of cellular prion protein (PrP
C
) in the brains of
CaBP-9k
-,
CaBP-28k
-, and
CaBP-9k/28k
-KO mice. PrP
C
expression was significantly upregulated in the brain of all three strains. Levels of phospho-Akt (Ser473) and phospho-Bad (Ser136) were significantly elevated, but those of phospho-ERK and phospho-Bad (Ser155 and 112) were significantly reduced in the brains of
CaBP-9k
-,
CaBP-28k
-, and
CaBP-9k/28k
-KO mice. The expressions of the Bcl-2, p53, Bax, Cu/Zn-SOD, and
Mn-SOD
proteins were decreased in the brains of all KO mice. Expression of the endoplasmic reticulum marker protein BiP/GRP78 was decreased, and that of the
CHOP
protein was increased in the brains of those KO mice. To identify the roles of
CaBP-28k
, we transfected PC12 cells with siRNA for
CaBP-28k
and found increased expression of the PrP
C
protein compared to the levels in control cells. These results suggest that
CaBP-28k
expression may regulate PrP
C
protein expression and these mice may be vulnerable to the influence of prion disease.
...
PMID:
Calbindin-D28k
in the Brain Influences the Expression of Cellular Prion Protein. 2954 46
