Introduction of LPAR3
LPAR3, also known as endothelial differentiation receptor 2 (EDG2) is a member of G protein-coupling receptor family and EDG subfamily. It is expressed in a lot of human tissues, but highly in specific tissues, such as prostate, testis, heart, urinary bladder and so on. Now most studies are designed to investigate the effect of LPAR3 on pathological process of many diseases and look forward to finding new potential therapeutic strategies for diseases.
|Basic Information of LPAR3|
|Protein Name||Lysophosphatidic acid receptor 3|
|Aliases||EDG7, GPCR, LPA3, Edg-7, LP-A3, HOFNH30, RP4-678I3|
|Organism||Homo sapiens (Human)|
Function of LPAR3 Membrane Protein
LPAR3 is involved in many biological functions via interacting with lysophosphatidic acid and mediating lysophosphatidic acid-evoked calcium mobilization. Most researches have been proved that LPAR3 is associated with the progression of types of cancers and atherosclerosis. LPAR1/3 antagonism can enhance the percentage of non-inflammatory, monocytes and T-regulatory cells and reduce LDL cholesterol levels, thus lowering atherosclerosis development. Moreover, LPAR3 is involved in the cell proliferation, apoptosis, invasion and migration. LPA stimulates the migration of oral carcinoma cells via LPAR3. In vivo study, the inhibition of LPA receptors can suppress migration and invasion in ovarian cancer cells. And Liao’s study shows LPA-LPA3 signaling pathway stimulates the activation of focal adhesion kinase (FAK) and paxillin, increasing cell motility in human pancreatic cancer cells. These findings also indicate LPA-LPAR3 axis can be considered as the potential therapeutic target for cancer and atherosclerosis. Besides, recent study indicates that LPA-LPAR3 axis is also related to the regulation of obesity via inhibiting insulin signaling in primary rat hepatocytes.
Fig.1 Schematic representation of the signaling pathways activated by the LPA1–6 receptors. (González-Gil, 2015)
Application of LPAR3 Membrane Protein in Literature
The study shows that osteoglycin (OGN) overexpression can significantly decrease the proliferation and migration of cardiac myofibroblasts (CMFs) and reduce the transactivation of the epidermal growth factor receptor (EGFR). Moreover, OGN interacts with LPA3 to suppress cell surface translocation of membrane type 1 matrix metalloproteinase (MT1-MMP) and subsequent pro-MMP-2 activation in Rho/ROCK-dependent manner, thus reducing EGFR transactivation.
The study indicates that LPA may interact with LPA1/3 and stimulates osteogenesis and angiogenesis capability of pre-osteoblasts, thus providing a novel and effective treatment strategy for bone regeneration success.
The study reveals that LPA3 may play a negative role during megakaryopoiesis in human hematopoietic stem cell and zebrafish, thus providing a new therapeutic strategy for megakaryopenia.
The study suggests that LPA1/3 receptor antagonists might be a potential new class of drugs that are suitable for treating or preventing alcohol use disorders.
The study uncovers that LPA signaling via LPA1 and LPA3 may be involved in the regulation of pancreatic cancer cells motile and invasive activities during tumor progression.
LPAR3 Preparation Options
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