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: EC:2.7.11.13 (
protein kinase C
)
49,245
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Periodontal disease, a frequent complication of diabetes mellitus, is the major cause of
tooth loss
. However, studies on neutrophil function in patients with this condition have yielded contradictory findings. The NADPH oxidase activity of 40 diabetic patients with periodontosis who were on metabolic control was evaluated and compared with that in 40 healthy subjects. Superoxide anion production was measured by a photometric method, with NBT reduction at 490 nm in a microplate reader and by a microscopic method, with a percentage of positive PMNs with granules of formazan in the cytoplasm. When the PMN respiratory burst was activated by phorbol myristate acetate (PMA), a
protein kinase C
(
PKC
) soluble activator, superoxide production of diabetics (4.31 +/- 1.67 A x 10(-3)/min) and normal subjects (4.25 +/- 1.25 A x 10(-3)/min) was comparable by photometric method, whereas a significantly defective response to opsonized zymosan was observed when the microscopic method was used (58 +/- 17% in diabetics and 66 +/- 18% in controls; p = 0.05). Therefore in patients with diabetes the impact on PMN function is of multifactorial origin, and is probably correlated to the glucose level and to glycation of PMN protein, such as NADPH oxidase or myeloperoxidase. Alternatively, glucose in PMN may be reduced by aldose reductase to polyols, and this pathway requires NADPH, the coenzyme for the respiratory burst. Moreover, we found that superoxide production in response to opsonized zymosan was reduced in diabetic patients. The activation of protein tyrosine kinase (PTK) is an important mechanism underlying transmembrane signaling and, moreover, protein tyrosine phosphorylations, stimulated by zymosan receptor-mediated activation, might be caused by the activation of specific PTK, whereas activation by PMA is probably mediated through another
PKC
type.
...
PMID:Respiratory burst of neutrophils in diabetic patients with periodontal disease. 970 64
Periodontitis is a chronic inflammatory disease that result in severe loss of supporting structures and substantial
tooth loss
. Oxidative stress is tightly involved in the progression of periodontitis. Tripartite Motif 16 (TRIM16) has been identified as a novel regulatory protein in response to oxidative and proteotoxic stresses. The present study aimed to investigate the role of TRIM16 in human periodontal ligament stem cells (hPDLSCs) under oxidative stress. First, we found that the expression of TRIM16 decreased after exposure to H
2
O
2
. Then TRIM16 overexpression alleviated H
2
O
2
-induced oxidative stress by enhancing antioxidant capacity and reducing the amount of intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS). TRIM16 increased cell viability, inhibited cell apoptosis and the depolarization of the mitochondrial membrane potential in hPDLSCs. Furthermore, TRIM16 attenuated H
2
O
2
-induced suppression of osteogenic differentiation. Mechanistically, TRIM16 promoted the activation of
protein kinase C
(
PKC
)-interacting cousin of thioredoxin (PICOT), p-Akt and Nrf2, while knockdown of PICOT reversed TRIM16-mediated ROS resistance and decreased the expression of p-Akt and Nrf2. In conclusion, TRIM16 alleviated oxidative damage in hPDLSCs via the activation of PICOT/Akt/Nrf2 pathway, suggesting that TRIM16 could be a promising target to develop effective therapies for periodontitis.
...
PMID:TRIM16 protects human periodontal ligament stem cells from oxidative stress-induced damage via activation of PICOT. 3309 21
