Ask about this productRelated genes to: SLC25A28 antibody
- Gene:
- SLC25A28 NIH gene
- Name:
- solute carrier family 25 member 28
- Previous symbol:
- -
- Synonyms:
- MRS3/4, MRS4L
- Chromosome:
- 10q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-19
- Date modifiied:
- 2016-02-18
Related products to: SLC25A28 antibody
Related articles to: SLC25A28 antibody
- Isoquercitrin (ISO), a neuroprotective flavonoid, alleviates ischemic stroke (IS) by inhibiting ferroptosis. In present study, we explored the mechanism of ISO attenuates neuronal ferroptosis in IS. - Source: PubMed
Publication date: 2026/08/03
Cai ShichangZhou SiqiWang YichengLi ZhenLong HongzhuChen YipingWu MeichunLi Xiuping - Seasonal crude protein (CP) and phosphorus (P) deficiency in northern Australian pastures reduces feed intake and growth of grazing ruminants, but the hepatic mitochondrial mechanisms underlying this response remain unclear. We characterized the hepatic mitochondrial transcriptome of sheep exposed to CP-P deficiency or matched-intake feed restriction. Merino wethers were assigned for 63 d to one of three treatments ( = 8/group): High CP-P, Low CP-P, or Restricted, in which High CP-P feed was offered at the same energy intake as the Low CP-P group. Liver RNA was sequenced, and transcripts encoding mitochondrial proteins were identified using MitoCarta 3.0. Differentially expressed genes (DEGs) were defined as adjusted < 0.05 and |log2FC| ≥ 0.585. Of 804 mitochondrial genes detected, 83 were differentially expressed in at least one pairwise comparison. The greatest transcriptional response occurred in contrasts against High CP-P (Low CP-P vs. High CP-P: 38 DEGs in 8 enriched pathways; Restricted vs. High CP-P: 37 DEGs in 10 enriched pathways). In both low-intake treatments, , , , and were upregulated, suggesting altered folate-mediated one-carbon metabolism. Restricted sheep also showed higher expression of several transporters (, , , , and ), indicative of enhanced mitochondrial nucleotide and metabolite exchange under CP-P adequate energy restriction. In contrast, Low CP-P sheep showed higher expression of and relative to either High CP-P or Restricted sheep, a nutrient-deficiency specific transporter response. expression was also higher in Restricted sheep than in both other groups. These findings suggest that reduced metabolizable energy intake was associated with the bulk of the hepatic mitochondrial transcriptional response, particularly in folate-mediated one-carbon metabolism, whereas CP-P deficiency was associated with a smaller but distinct transporter signature. The liver mitochondrial transcriptome may provide mechanistic insight into nutritional adaptation under CP and P deficiency in grazing sheep. - Source: PubMed
Publication date: 2026/05/31
Fernandez Elmer EInnes David JBottje Walter GFortes Marina R SPoppi Dennis PQuigley Simon PBond Jude JHudson Nicholas J - Mitochondrial dysfunction plays a central role in the pathogenesis of bronchopulmonary dysplasia (BPD). Solute carrier family 25 member 28 (SLC25A28) is an iron transporter located in the inner mitochondrial membrane. In this study, we aimed to explore the role and underlying molecular mechanisms of SLC25A28 in BPD. Hyperoxia (85% O) was used to establish a neonatal murine model of BPD, and mouse lung epithelial cells (MLE-12 cells) were used in vitro. SLC25A28 expression and activity were downregulated under hyperoxic conditions, both in vivo and in vitro. SLC25A28 overexpression restored hyperoxia-induced mitochondrial oxidative phosphorylation (OXPHOS) dysfunction, and further enhanced the proportion of Ki67-positive cells by 37% ( < 0.05) and increased migration by 33% ( < 0.01) in MLE-12 cells. In contrast, SLC25A28 knockdown exacerbated these impairments in MLE-12 cells, with reduced the proportion of Ki67 positive cells by 71% ( < 0.01) and a 35% reduction in the migration rate. SLC25A28 was also knocked down in vivo, which further aggravated alveolar simplification in BPD mice. Furthermore, the mitochondrial-targeted peptide SS-31 could potentially interact with SLC25A28 and preserve its protein abundance. SS-31 administration mitigated hyperoxia-induced alveolar simplification, with the radical alveolar count (RAC) increasing by 28% ( < 0.05) and the mean linear intercept (MLI) decreasing by 20% ( < 0.001). In summary, this study revealed that SLC25A28 ameliorated hyperoxic lung injury by improving mitochondrial OXPHOS in alveolar epithelial cells, suggesting that it may serve as a potential therapeutic target for BPD. - Source: PubMed
Publication date: 2026/04/08
Lu TaoChen Shi-QiLi Shu-HongLi Sheng-PengWu Ya-XianPang Qing-FengChen Dan - Nitrite accumulation poses a significant threat to aquatic organisms in intensive aquaculture systems. Macrobrachium rosenbergii, a commercially vital freshwater prawn, exhibits adaptive responses to environmental stressors, yet the molecular mechanisms underlying nitrite tolerance remain poorly understood. This study employed integrated mRNA and miRNA transcriptomics to dissect the regulatory networks activated in M. rosenbergii hepatopancreas under acute nitrite stress (0, 40, and 87.25 mg/L nitrite-N over 48 h). High-throughput sequencing revealed 640 and 912 differentially expressed genes (DEGs) in low-concentration (LC) and high-concentration (HC) groups, respectively, compared to controls (CK). In the LC group, enrichment was predominantly observed in ribosome biogenesis (96 genes, p < 0.001). Conversely, the HC group was characterized by the significant modulation of the PPAR signaling (11 genes), glycerophospholipid metabolism, and the citrate cycle (p < 0.005). Calcium signaling and MAPK pathways may be central to stress adaptation across both groups. miRNA profiling revealed 17 downregulated and 2 upregulated miRNAs within the HC group relative to the CK group, with miR-193-y, miR-263-x, and miR-145-x implicated in metabolic regulation. Notably, novel miRNAs (e.g., novel-m0087-3p) showed concentration-dependent expression. qPCR validated the consistency of sequencing data, confirming stress-responsive genes (P53, HORMA, SLC25a28) and miRNAs. This study is the first to integrate the mRNA-miRNA regulatory network in Macrobrachium rosenbergii to elucidate the response mechanism to nitrite stress, emphasizing the role of metabolic reprogramming and signal pathway regulation as key survival strategies. It provides a foundation and novel perspectives for the molecular evolution of nitrite adaptability in aquatic animals and breeding programs. - Source: PubMed
Publication date: 2026/03/04
Li XilianCheng HaihuaFan YunpengXu BinpengXu YangGao Qiang - Postoperative cognitive dysfunction is a type of cognitive impairment that occurs after surgery. Here, this experiment investigated the role of PLCG1 in sevoflurane-induced model and the molecular mechanisms underlying its regulation of ferroptosis. Single-cell RNA sequencing data and bioinformatic analyses were performed using GEO datasets (GSE196239). Mice were exposed to 2.3% sevoflurane for 2 h daily for 3 consecutive days. PLCG1 expression was up-regulation in patients exposed to sevoflurane. Specifically, blood samples from these patients exhibited elevated levels of PLCG1 mRNA. Consistently, in a mouse model of sevoflurane exposure, both mRNA and protein levels of PLCG1 were significantlyincreased in brain tissue. Single-cell RNA sequencing analysis revealed that PLCG1 was predominantly expressed in astrocytes (marked by AQP4, GFAP, LUZP2, and SLC25A28) and neurons (marked by B3GAT2, ENO2, GNG2, and SLC1A1) in sevoflurane-exposed patients. In contrast, PLCG1 expression was undetectable in B cells (CD74, CD79B, CD80, CD86), T cells (CD4, CD8B, CD69, CD247), or macrophages (CD36, CD68, CD83, CD163). In conclusion, PLCG1 drives neuronal ferroptosis in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. In conclusion, PLCG1 drives neuronal in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A Ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. - Source: PubMed
Publication date: 2026/02/27
Chen JianCai YangWang JingruYue KunSun Yingying