Ask about this productRelated genes to: SERPINB6 Blocking Peptide
- Gene:
- SERPINB6 NIH gene
- Name:
- serpin family B member 6
- Previous symbol:
- PI6, DFNB91
- Synonyms:
- PTI, CAP
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-20
- Date modifiied:
- 2016-04-06
Related products to: SERPINB6 Blocking Peptide
Related articles to: SERPINB6 Blocking Peptide
- Postoperative pain remains a major perioperative challenge, with undermanagement leading to delayed recovery, poor patient satisfaction, morbidity and the potential development of chronic pain. Perioperative dietary intake, such as a high-fat diet (HFD), has emerged as an essential regulator of postoperative pain sensitivity. While long-term HFD induces direct neuronal sensitization to prolong pain responses, the impact of short-term HFD on perioperative pain and its underlying mechanisms is yet to be characterized. Here, we investigated the role of short-term HFD intervention in postoperative pain using the hindpaw incision (HPI) model in male mice. Pain behavioral tests showed that two weeks of HFD exposure significantly prolonged mechanical and thermal nociceptive responses in HPI compared to the normal diet. Mechanistically, short-term HFD disrupted lipid metabolic homeostasis, which dysregulated the local immune microenvironment. It shifted macrophage polarization from anti-inflammatory M2 to pro-inflammatory M1 phenotype and upregulated pro-nociceptive cytokines (e.g., TNF-α, IL-6) in the incised paw tissues. Notably, SerpinB6, a key mediator linking lipid metabolism to immune regulation, was downregulated by short-term HFD. Local restoration of SerpinB6 normalized macrophage polarization, reduced pro-inflammatory cytokines (IL-6, TNF-α), and alleviated pain hypersensitivity. Furthermore, SerpinB6 exerted its effect by restoring Sirt1 expression and attenuating ERK phosphorylation. Collectively, our findings revealed that short-term HFD primed acute postoperative pain via SerpinB6 protein downregulation and subsequent immune microenvironment dysregulation. This study highlighted that short-term dietary intervention and SerpinB6 are potential therapeutic strategies for perioperative pain management. - Source: PubMed
Publication date: 2026/07/11
Liu JingjingMeng FeiLiao BoyaGu Chris Kwan YinLiu Aijia JessicaJiao YingfuWong Stanley Sau Ching - Asthma is a multifactorial disease with a role of genetic susceptibility and environmental exposures. These aspects are poorly understood for pediatric obesity-related asthma, a phenotype of non-allergic asthma. - Source: PubMed
Publication date: 2026/06/22
Thompson David AWabara Yvonne BDuran SaraiReichenbach AnnaRastogi Deepa - We examined gene expression profiles in abdominal aortic aneurysm (AAA) lesions . normal aortas by cDNA microarray and real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR). - Source: PubMed
Lu SongLi Li PingWhite John VZhang XiaoyingNwaneshiudu IfeyinwaNwaneshiudu AdaobiNtaoula NectariaGaughan JohnMonos Dimitri SLin Wan-LuSolomides Charalambos COleszak Emilia LPlatsoucas Chris D - Adaptive immune responses play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS). In this study, we investigated the functional mechanisms of T cell subtypes and assessed the causal links between CD4+ cytotoxic T cell-related genes and ALS risk. - Source: PubMed
Pang Xin YuanWang Hong FenBai Jiong MingHuang Xu Sheng - Hereditary deafness accounts for 60% of congenital hearing loss, and more than 300 deafness genes have been identified. SERPINB6, a gene associated with recessive deafness, also named DFNB91, is linked to non-syndromic progressive hearing loss based on studies of humans and its mouse ortholog Serpinb6a knockout mice. However, the mechanism and biological therapy for SERPINB6 mutation-induced deafness remain unknown. Here, we demonstrate that Gch1 is aberrantly overexpressed in Serpinb6a-deficient hair cells. Upregulation of Gch1 in wild-type mice cochlea via adeno-associated virus (AAV) resulted in hearing loss and hair cell death, while downregulation of GCH1 by its inhibitor DAHP effectively protected hair cells and auditory function in Serpinb6a knockout mice. Dysregulation of the Serpinb6a/Gch1 axis resulted in elevated expression of BH4 and then iNOS, leading to increased ROS production and eventually causing hair cell damage. These findings revealed that Gch1 overexpression is the mechanism underlying deafness induced by Serpinb6a mutation. Critically, Myo15 promoter-driven AAV delivery of exogenous Serpinb6a effectively rescues auditory function and hair cell survival in Serpinb6a-deficient mice. These findings suggested that AAV-based gene therapy offers a potential treatment for Serpinb6a knockout mice, which may serve as a promising strategy for treating DFNB91 patients in clinical settings. - Source: PubMed
Publication date: 2026/01/29
Cheng ChengZhang LiyanLu JieTan FangzhiHuang YidengGao SongLi SiyuQiu YueHao WenliZhou YingyiLu JunzeJi XinyaLi AoZhang XinruFan JinyiLi HeQian XiaoyunQi JieyuGao XiaChai Renjie