Ask about this productRelated genes to: LPAR3 antibody
- Gene:
- LPAR3 NIH gene
- Name:
- lysophosphatidic acid receptor 3
- Previous symbol:
- EDG7
- Synonyms:
- LP-A3, Edg-7, RP4-678I3, HOFNH30, LPA3
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-02
- Date modifiied:
- 2014-11-19
Related products to: LPAR3 antibody
Related articles to: LPAR3 antibody
- Temporomandibular disorders (TMD) pain is the most common orofacial pain with limited effective treatments. Here, we observed elevated lysophosphatidic acid (LPA), a bioactive lipid, in blood, trigeminal ganglion (TG), and peri-temporomandibular joint (TMJ) tissues in mouse models of TMD-like pain induced by TMJ inflammation or masseter muscle injury. Notably, LPA levels were also elevated in TMD patients' blood and positively correlated with their pain intensity. LPA receptors (LPAR) 1 and 3 were expressed in mouse and human TG neurons and upregulated in TMD-like pain models. Inhibition or knockout of LPAR1 or LPAR3 attenuated TMD-like pain, while LPA injection into the TMJ or masseter muscle evoked pain. Furthermore, we demonstrated that LPA/LPAR signaling upregulates and sensitizes PIEZO2, a mechanosensitive ion channel, in TG neurons via extracellular signal-regulated kinase (ERK). Specific deletion or inhibition of PIEZO2 and suppression of ERK activation in TG neurons mitigated TMD-like pain. These findings suggest that LPA/LPAR signaling drives TMD-like pain via PIEZO2, offering potential therapeutic targets. - Source: PubMed
Publication date: 2026/07/23
Zhang QiaojuanSu ShanchunLiang PengfeiChen YunKim MinseokBaldi RobertWang PengDias Fabiana CJang MinjiGonzalez Torres Maria ALim PeifengMoreira Roger W FChun JeroldGuilak FarshidYang HuangheLiedtke WolfgangNackley AndreaChen Yong - The Karan Fries (KF), a newly developed dairy cattle (Holstein Friesian × Tharparkar), after nine generations of inter se mating (mating among crossbreds) by maintaining a stable, composite breed structure, is expected to preserve some heterosis or hybrid vigour through the retention of heterozygosity and selective pressure for performance traits. Although a decline in productivity is generally seen from F1 to later inter se generations, the rate of loss of heterosis slows down, allowing the population to reach a new equilibrium. This seems to be an interesting proposition. Therefore, to assess the retained heterosis and to evaluate the current status of the KF population, the present study was conducted, which included a sizeable phenotyped and genotyped animals (n = 355). The analysis identified a stabilized genomic architecture with a mean exotic inheritance of 64.34 ± 0.74% (predominantly Holstein Friesian) and an indigenous contribution of 35.66 ± 0.95% (primarily Tharparkar). Genomic indicators of heterosis revealed a mean Genomic Retained Heterosis (RH) of 59% which accounts for 15.82% of the total observed KF average yield (4153.14 ± 167.32 kg). Genomic Retained Heterozygosity (RHET) of 0.44%. Notably, a near-perfect correlation (r = 0.98) was observed between these two metrics, indicating that RHET can be used interchangeably with RH to assess heterosis and its effects in instances where parental genotypic records were absent. Linear regression analysis demonstrated that RH was a primary driver of productivity, with Total Milk Yield (TMY) increasing by 1113.81 ± 301.91 kg per unit increase in RH (p < 0.001). The impact on TMY was significantly larger than on 305-day milk yield (339.08 ± 282.92 kg), suggesting that genomic heterosis specifically enhances lactation persistence and environmental robustness. A joint-model GWAS identified 182 SNPs with significant additive effects and 117 SNPs with significant dominance effects for TMY. Functional annotation revels candidate genes for milk synthesis (SLC25A1, PIP4K2A, LATS2), heat stress resilience (DNAJB5, DNAJC1), and immunological defence (ARHGAP15, LPAR3). Protein network analysis identified the Mitochondrial Ribosomal Protein (MRP) family, specifically hub gene MRPL22, as the central driving gene for both additive and dominance components. These findings confirm that KF cattle effectively leverage retained heterosis to integrate high production potential with robust tropical climatic adaptability. - Source: PubMed
Publication date: 2026/07/20
Kumar IshmeetVyas JayeshKhan AsadRamola GargiIlayaraja IMuansangi LalChitra AnilPal PritamSingh Ritik KumarKamboj M LRaja T VMukherjee AnupamaMukherjee Sabyasachi - Chronic exposure to ultraviolet B (UVB) radiation induces excessive reactive oxygen species (ROS) production in dermal fibroblasts, leading to cellular senescence and skin photoaging. Ageing skin is characterised by disruption of the immune microenvironment, including impaired macrophage polarisation and reduced M2 macrophage activity. However, the contribution of M2 macrophages to fibroblast photoaging remains incompletely understood. Here, we investigated whether M2 macrophages attenuate UVB-induced fibroblast senescence through ectonucleotide pyrophosphatase/phosphodiesterase 2 (ENPP2)-dependent lysophosphatidic acid (LPA)signalling. UVB-induced L929 fibroblasts were treated with conditioned media derived from polarised RAW264.7 macrophages, with or without ENPP2 silencing. UVB exposure induced marked senescence, oxidative stress, and mitophagy impairment, whereas conditioned medium from M2 macrophages significantly alleviated these effects compared with M1-derived conditioned medium. Notably, ENPP2 depletion in M2 macrophages substantially reduced these protective effects. M2 macrophage-derived conditioned medium contained elevated LPA levels and restored UVB-suppressed LPAR1 and LPAR3 expression in fibroblasts. Pharmacological inhibition of LPAR1/3 attenuated the protective effects of M2 macrophages, while exogenous LPA supplementation restored these effects under ENPP2-deficient conditions. These changes were associated with enhanced PINK1/Parkin-related mitophagy signalling and reduced oxidative stress. Collectively, these findings identify M2 macrophage-derived ENPP2/LPA signalling as a critical paracrine mechanism that mitigates UVB-induced fibroblast photoaging. - Source: PubMed
Lu MeiqiWang XiaoyangHu YujieJia ShanshanQi YongjunJiao YaZhao JieWang XiaochuanZhang JixunJiang Duyin - Endotoxemia represents a life-threatening clinical disorder driven by an aberrant host immune response to pathogenic infection, often resulting in severe multiple organ dysfunction. Among its most devastating complications are acute lung injury (ALI) and endotoxemia-associated encephalopathy (EAE), both of which are associated with elevated mortality and currently lack effective targeted interventions. This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia. Our results showed that treatment with rhTβ4 markedly enhanced survival rates and diminished the systemic overproduction of diverse proinflammatory cytokines and chemokines in endotoxemic mice. These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress. Moreover, rhTβ4 treatment significantly rescued EAE-related cognitive deficits and attenuated neuronal damage, primarily through the suppression of neuroinflammation and microglial overactivation. Integrative transcriptomic profiling and functional assays identified lysophosphatidic acid receptor 3 (LPAR3) as an important contributor, suggesting that rhTβ4 suppresses microglial-mediated neurotoxicity at least in part through LPAR3 downregulation. In conclusion, rhTβ4 confers robust multi-organ protection against endotoxemic injury by orchestrating the inhibition of systemic and central neuroinflammatory cascades, positioning it as a promising candidate for the treatment of endotoxemia-induced ALI and EAE. - Source: PubMed
Publication date: 2026/05/22
Ye YumengYang XuefengLiu YingZhao JingshuoChen TongtongXing YujieZuo HongyanHao YanhuiLi Yang - The aim of the present study was to explore the reparative effects of spermidine combined with umbilical cord mesenchymal stem cells (UC-MSCs) on endometrial injury in mice. First, bioinformatic results suggested that endometrial damage is closely linked to immune mechanisms, a finding that was corroborated by quantitative polymerase chain reaction results. Next, an endometrial injury model was established by injecting 95% ethanol into the uterus, and spermidine combined with UC-MSCs was used for treatment. We found that the combination of spermidine and umbilical cord mesenchymal stem cells (S+UC-MSCs) significantly reduced CD36 expression while significantly increasing the expression of the proteins THBS2, TIMP3, CLU, and CFH. In addition, S + UC-MSCs significantly increased the number of Tregs and the protein levels of interleukin-4 (IL-4) and interleukin-10 (IL-10), whereas the protein levels of interleukin-6 (IL-6), interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), interleukin-2 (IL-2), and interleukin-17 (IL-17) decreased significantly. Furthermore, S + UC-MSCs also improved the morphology of mouse endometria by regulating angiogenesis (microvessel density [MVD] and vascular endothelial growth factor [VEGF]) and receptivity (HOXA10, LIF, LPAR3, and αvβ3). These results indicated that the combined therapy of spermidine and UC-MSCs promotes angiogenesis, enhances uterine receptivity, regulates the IL-10/Treg-mediated immune microenvironment to restore endometrial morphology, and shows a tendency to increase the pregnancy rate in mice. - Source: PubMed
Publication date: 2026/06/24
Sun KaiheLin XiuyingNiu ChunxueMi XuguangChen ShilingJin Dan