2012
DOI: 10.1016/j.jsbmb.2012.03.001
|View full text |Cite
|
Sign up to set email alerts
|

Phospholipase A2 activating protein is required for 1α,25-dihydroxyvitamin D3 dependent rapid activation of protein kinase C via Pdia3

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

3
33
0

Year Published

2013
2013
2024
2024

Publication Types

Select...
5
2
1

Relationship

3
5

Authors

Journals

citations
Cited by 35 publications
(37 citation statements)
references
References 37 publications
(57 reference statements)
3
33
0
Order By: Relevance
“…Our current study provides the first evidence from immunohistochemistry that shockwave therapy can induce articular cartilages expression of Pdia-3, the critical transcription factor responsible for the matrix formation of chondrocyte. Recent studies reported that 1α,25(OH)2D3 rapidly stimulated membrane signaling via Pdia-3 dependent activation in growth zone chondrocytes and promotes the production of matrix protein [11,13,20,22,42,43]. The present study showed the decrease of cartilage matrix loss and increased aggrecan and collagen II expression in shockwave group.…”
Section: Discussionsupporting
confidence: 62%
See 1 more Smart Citation
“…Our current study provides the first evidence from immunohistochemistry that shockwave therapy can induce articular cartilages expression of Pdia-3, the critical transcription factor responsible for the matrix formation of chondrocyte. Recent studies reported that 1α,25(OH)2D3 rapidly stimulated membrane signaling via Pdia-3 dependent activation in growth zone chondrocytes and promotes the production of matrix protein [11,13,20,22,42,43]. The present study showed the decrease of cartilage matrix loss and increased aggrecan and collagen II expression in shockwave group.…”
Section: Discussionsupporting
confidence: 62%
“…Extracellular signal-regulated kinases (ERKs), acted as an integration point for multiple biochemical signals, and were involved in an osteoblast cellular processes such as proliferation, differentiation, transcription regulation and development [12,22]. Upon activation by Pdia-3 after ESWT, these kinases translocations to the nucleus of the osteoblast cells, where it phosphorylated nuclear targets.…”
Section: The Expression Of Pdia-3 and Extracellular Signal-regulated mentioning
confidence: 99%
“…In vitro and in vivo studies have confirmed the expression of PLAA mRNA in the region of the growth plate that is sensitive to 1a,25(OH) 2 D 3 [35]. 1a,25 (OH) 2 D 3 treatment triggers the interaction between PLAA and Pdia3 receptor complex in osteoblasts and chondrocytes [16]. Moreover, silenced PLAA (ShPlaa) osteoblasts fail to rapidly activate PKC and PLA 2 in response to 1a,25(OH) 2 D 3 treatment [16].…”
Section: Wnt5a Signals Via the Camkii/pla 2 /Pge 2 /Pkc Cascadementioning
confidence: 81%
“…1a,25(OH) 2 D 3 initiates its effects via Pdia3 localized in caveolae plasma membrane domains [6,9]. The binding of 1a,25(OH) 2 D 3 to Pdia3 stimulates the interaction between Pdia3 and phospholipase-A 2 (PLA 2 )-activating protein (PLAA) [16], triggering the activation of calcium/calmodulindependent protein kinase II (CaMKII) [17]. Next, PLA 2 is activated [18], generating lysophospholipid and releasing arachidonic acid (AA) [19].…”
mentioning
confidence: 99%
“…Arachidonic acid can activate PKC directly through a PLAA mediated pathway or be further metabolized, resulting in PGE 2 production, which then acts through its EP1 receptor leading to MAPK activation. Alternatively, IP 3 stimulates Ca +2 release from the endoplasmic reticulum and activation of PKCα via translocation to the plasma membrane by DAG [38,74] (Fig. 1).…”
Section: Rapid Non-genomic Membrane Signalingmentioning
confidence: 99%