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Genetic inactivation of TRPM4 does not alter the temperature-dependent movement of mouse microglia. TRPM4基因失活不会改变小鼠小胶质细胞的温度依赖性运动。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-03-10 DOI: 10.1016/j.jphyss.2026.100067
Rei Nishimoto, Yoshikazu Matsuoka, Makoto Tominaga
{"title":"Genetic inactivation of TRPM4 does not alter the temperature-dependent movement of mouse microglia.","authors":"Rei Nishimoto, Yoshikazu Matsuoka, Makoto Tominaga","doi":"10.1016/j.jphyss.2026.100067","DOIUrl":"10.1016/j.jphyss.2026.100067","url":null,"abstract":"<p><p>Temperature sensing shapes behavior and cellular functions, yet the molecular basis of thermosensitivity in non-neuronal cells remains poorly defined. Microglia are resident immune cells of the central nervous system that help maintain brain homeostasis via immune surveillance and injury responses. We previously showed that microglial motility is temperature dependent and is largely mediated by the thermosensitive ion channel transient receptor potential vanilloid 4 (TRPV4), a thermosensitive ion channel. However, the contribution of transient receptor potential melastatin 4 (TRPM4) is unclear because suitable Trpm4 mutant mice were not available in our earlier work. Here, we generated functional Trpm4-knockout mice (TRPM4KO) using CRISPR/Cas9 genome editing based on a published strategy. Time-lapse imaging of primary microglia across a range of temperatures revealed that Trpm4 deficiency did not alter temperature-dependent motility in vitro. These results indicate that TRPM4 is dispensable for temperature-dependent microglial motility.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100067"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12999298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Involvement of interaction between TRPM2 and IKCA1 in temperature-dependent movement and IL-1β production in mouse microglia. TRPM2和IKCA1在小鼠小胶质细胞温度依赖性运动和IL-1β产生中的相互作用。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-05-01 DOI: 10.1016/j.jphyss.2026.100077
Aykut Deveci, Makiko Kashio, Sandra Derouiche, Jing Lei, Yuji Imaizumi, Susumu Ohya, Moe Iwata, Makoto Tominaga
{"title":"Involvement of interaction between TRPM2 and IKCA1 in temperature-dependent movement and IL-1β production in mouse microglia.","authors":"Aykut Deveci, Makiko Kashio, Sandra Derouiche, Jing Lei, Yuji Imaizumi, Susumu Ohya, Moe Iwata, Makoto Tominaga","doi":"10.1016/j.jphyss.2026.100077","DOIUrl":"10.1016/j.jphyss.2026.100077","url":null,"abstract":"<p><p>Transient potential melastatin 2 (TRPM2) plays important roles in Ca<sup>2 +</sup> signaling in tissues and cells, and contributes to various cellular functions. The Ca<sup>2+</sup> influx induced by TRPM2 may activate the intermediate conductance Ca<sup>2+</sup>-activated potassium channel (IKCA1/ K<sub>Ca</sub>3.1/ SK4) and trigger K<sup>+</sup> efflux. Here we demonstrate that a functional interaction between TRPM2 and IKCA1 contributes to cell volume changes in HEK293T cells and mouse primary microglia. Ca<sup>2+</sup> entering cells through TRPM2 causes K<sup>+</sup> efflux, followed by cell shrinkage upon water efflux. In addition, mouse microglia exhibited temperature-dependent movement in vitro that was modulated by the TRPM2-IKCA1 interaction within the physiological body temperature range. This interaction was also found to be involved in cytokine production in microglia. Understanding how the TRPM2-IKCA1 interaction in microglia can promote cell movement and cytokine production could be valuable for developing new strategies for treatments of diseases involving TRPM2.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100077"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Changes in palmitate- and stearate-containing glycerophospholipids in skeletal muscle during clenbuterol-induced fast-twitch fiber transition and hypertrophy. 瘦肉精诱导的快肌纤维转换和肥厚过程中骨骼肌中棕榈酸酯和硬脂酸酯类甘油磷脂的变化。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-05-21 DOI: 10.1016/j.jphyss.2026.100081
Yuna Suzuki, Tomoki Sato, Satoshi Ohuchi, Sango Nakashima, Noriyuki Miyoshi, Shinji Miura
{"title":"Changes in palmitate- and stearate-containing glycerophospholipids in skeletal muscle during clenbuterol-induced fast-twitch fiber transition and hypertrophy.","authors":"Yuna Suzuki, Tomoki Sato, Satoshi Ohuchi, Sango Nakashima, Noriyuki Miyoshi, Shinji Miura","doi":"10.1016/j.jphyss.2026.100081","DOIUrl":"10.1016/j.jphyss.2026.100081","url":null,"abstract":"<p><p>Fast- and slow-twitch skeletal muscle fibers exhibit distinct glycerophospholipid compositions, and slow-twitch transition is accompanied by characteristic changes in glycerophospholipid molecular species. However, whether glycerophospholipid composition is remodeled during fast-twitch fiber transition and skeletal muscle hypertrophy remains unclear. In this study, we examined changes in palmitate- and stearate-containing glycerophospholipids using a mouse model of clenbuterol-induced fast-twitch transition and hypertrophy. Clenbuterol administration increased the proportion of fast-twitch fibers and induced skeletal muscle hypertrophy. Lipidomic analysis revealed a significant increase in palmitate-containing phosphatidylcholine and a decrease in stearate-containing phosphatidylcholine in the tibialis anterior and soleus muscles. Consistent with these glycerophospholipid alterations, the expression of several acyltransferases, such as glycerol-3-phosphate acyltransferase 3 (GPAT3), involved in glycerophospholipid acyl-chain determination was significantly altered. These findings demonstrate that glycerophospholipid composition is remodeled during fast-twitch fiber transition and muscle hypertrophy, highlighting lipid remodeling as a component of skeletal muscle phenotypic adaptation.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100081"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13234236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Attentional modulation of sensory gating during a visuomotor task. 视觉运动任务中感觉门控的注意调节。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-05-15 DOI: 10.1016/j.jphyss.2026.100080
Cuong Nguyen Van, Duc Le Trung, Takeru Okamoto, Masataka Tatsumi, Thu Nguyen Dang, Yuya Hyodo, Satoshi Kase, Tomoyuki Kurose, Takeshi Imura, Hisao Nishijo, Susumu Urakawa
{"title":"Attentional modulation of sensory gating during a visuomotor task.","authors":"Cuong Nguyen Van, Duc Le Trung, Takeru Okamoto, Masataka Tatsumi, Thu Nguyen Dang, Yuya Hyodo, Satoshi Kase, Tomoyuki Kurose, Takeshi Imura, Hisao Nishijo, Susumu Urakawa","doi":"10.1016/j.jphyss.2026.100080","DOIUrl":"10.1016/j.jphyss.2026.100080","url":null,"abstract":"<p><p>Attention is crucial for motor performance because it enhances task-relevant processing while suppressing distractions. However, physiological markers of attentional engagement during motor activity remain incompletely understood. The present study investigated how attention modulates sensory gating (SG) along with heart rate variability (HRV) and eye blink rate (EBR) during a visual cue-based typing task. Twenty-five participants performed under three conditions: (1) no typing, (2) free typing, (3) precision typing. The results revealed that higher attention led to a consistent increase in SG across distinct modalities. Particularly, this modulation was observed in higher-order components: N1, P2 in auditory evoked potential; P1 in visual evoked potential; P2, P3 in somatosensory evoked potential. Furthermore, task-related HRV modulation was associated with varying attentional and motor demands, while EBR decreased with increased visual attentional engagement. These findings further clarify SG and autonomic changes during attentional modulation in motor tasks, highlighting their potential for assessing attentional engagement.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100080"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13199777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Slow and fast locomotor muscle adaptations to sustained intermittent hypoxaemia. 慢速和快速运动肌肉对持续间歇性低氧血症的适应。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-06-20 DOI: 10.1016/j.jphyss.2026.100084
Lise Paprzycki, Vincianne Jenart, Alexandre Legrand, Carine Michiels, Alexandra Tassin
{"title":"Slow and fast locomotor muscle adaptations to sustained intermittent hypoxaemia.","authors":"Lise Paprzycki, Vincianne Jenart, Alexandre Legrand, Carine Michiels, Alexandra Tassin","doi":"10.1016/j.jphyss.2026.100084","DOIUrl":"10.1016/j.jphyss.2026.100084","url":null,"abstract":"<p><p>Episodic hypoxaemia is associated with muscle dysfunction in respiratory insufficiencies, but its effects depend on the hypoxia/reoxygenation pattern. Sustained Intermittent Hypoxemia (SIH) characterizes a large subgroup of COPD patients, yet muscle adaptations to SIH remain poorly known. We used a mouse model of SIH (FiO₂: 10%, 8 h/day) and analysed myofibre structure, muscle mass regulators, and myogenic markers in fast and slow-twitch hindlimb muscles. SIH induced an increase in haematocrit. At 35 days, Soleus cross-sectional area increased predominantly in slow-twitch fibres, but not in the fast Tibialis Anterior (TA) muscle. HIF1 target gene expression was increased at early timepoints with muscle-type-specific differences. While myostatin plasma levels were decreased, myostatin receptor and atrogene expression differed between muscles at baseline and upon SIH. Myod1 and Myog expression decreased over time in the TA only. In conclusion, SIH induces muscle-type-specific adaptations, promoting hypertrophy in slow-twitch muscle while impairing myogenic regulation in fast-twitch muscle.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100084"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13333354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148330401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dynamic regulation of TASK-1 channels under cellular stress. 细胞应激下TASK-1通道的动态调控。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-03-14 DOI: 10.1016/j.jphyss.2026.100069
Yang Yu, John Curry, Sarah Tankersley, Keli Hu
{"title":"Dynamic regulation of TASK-1 channels under cellular stress.","authors":"Yang Yu, John Curry, Sarah Tankersley, Keli Hu","doi":"10.1016/j.jphyss.2026.100069","DOIUrl":"10.1016/j.jphyss.2026.100069","url":null,"abstract":"<p><p>TASK-1 channel is important for regulating membrane potential. However, its response to pathological conditions remains unknown. In this study, we investigated the effects of hypoxia on the recombinant TASK-1 channel localization at the surface of HEK293T cells. The hypoxic condition was induced via sodium cyanide (NaCN) treatment. Exposure to NaCN led to a significant decrease in TASK-1 levels at the cell surface. This reduction was blocked by pre-exposure to a selective protein kinase C (PKC) inhibitor bisindolylmaleimide. Additional experiments demonstrated that blocking dynamin function or depleting cellular cholesterol prevented TASK-1 from the reduction at the cell surface. Fluorescence microscopic analysis further showed a selective reduction in cell surface wild type TASK-1 under hypoxic conditions, while double-leucine mutant TASK-1 remained unchanged. These results reveal a novel mechanism by which TASK-1 channel localization is modulated by chemical hypoxia, highlighting the importance of PKC, dynamin, and cholesterol in regulating TASK-1 trafficking.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100069"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147486434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sweat components as a promising monitoring tool for systemic diseases. 汗液成分作为一种有前途的全身性疾病监测工具。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-03-15 DOI: 10.1016/j.jphyss.2026.100068
Changqi Shi, Ziyi Chen, LuLu Zhang, Xiaomeng Zhang, Xiaoyu Liang, Lan Yan, Xiaopeng Hao, Guoju Dong, Cheng Lu, Luqi Huang
{"title":"Sweat components as a promising monitoring tool for systemic diseases.","authors":"Changqi Shi, Ziyi Chen, LuLu Zhang, Xiaomeng Zhang, Xiaoyu Liang, Lan Yan, Xiaopeng Hao, Guoju Dong, Cheng Lu, Luqi Huang","doi":"10.1016/j.jphyss.2026.100068","DOIUrl":"10.1016/j.jphyss.2026.100068","url":null,"abstract":"<p><p>Sweat is a complex biological fluid primarily responsible for thermoregulation, containing diverse organic and inorganic components derived from plasma and interstitial fluids. Its secretion is tightly regulated by hypothalamic-sympathetic pathways and reflects systemic physiological status. Recent studies reveal that sweat composition dynamically changes with various systemic diseases, providing diagnostic, mechanistic, and prognostic insights. Abnormalities in sweat components, such as electrolytes, glucose, lactate, amino acids, and proteins, mirror underlying metabolic, endocrine, immune, and neural dysregulation. This review synthesizes current evidence on how these alterations arise from specific physiological mechanisms-including transdermal diffusion, transporter-mediated secretion (e.g., GLUT2, CFTR), ductal reabsorption, and autonomic control-linking sweat gland biology to systemic homeostasis. These insights support the clinical development of sweat as a non-invasive biofluid for disease monitoring.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100068"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147486452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Weight loss by sodium-glucose co-transporter 2 inhibitor canagliflozin is followed by rebound in db/db mice but maintained in fat-fed mice via circadian rises in body temperature and locomotor activity. 钠-葡萄糖共转运蛋白2抑制剂canagliflozin在db/db小鼠中体重减轻后会反弹,但在脂肪喂养小鼠中通过体温和运动活动的昼夜节律升高来维持体重。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-05-14 DOI: 10.1016/j.jphyss.2026.100079
Lei Wang, Wanxin Han, Dauren Zhantleu, Seiya Banno, Yermek Rakhat, Nazymgul Kulzhanova, Abilkhair Yussupov, Yusaku Iwasaki, Masanori Nakata, Daisuke Yabe, Yutaka Seino, Toshihiko Yada
{"title":"Weight loss by sodium-glucose co-transporter 2 inhibitor canagliflozin is followed by rebound in db/db mice but maintained in fat-fed mice via circadian rises in body temperature and locomotor activity.","authors":"Lei Wang, Wanxin Han, Dauren Zhantleu, Seiya Banno, Yermek Rakhat, Nazymgul Kulzhanova, Abilkhair Yussupov, Yusaku Iwasaki, Masanori Nakata, Daisuke Yabe, Yutaka Seino, Toshihiko Yada","doi":"10.1016/j.jphyss.2026.100079","DOIUrl":"10.1016/j.jphyss.2026.100079","url":null,"abstract":"<p><p>Sodium-glucose co-transporter 2 (SGLT2) inhibitors, diabetic medicines, induce glucosuria to lower glycemia and energy reserve, initially reducing weight. The weight-reducing capacity substantially differs between individuals, likely due to both social/psychological factors and physical/metabolic states. Exclusively analyzing the contribution of physical/metabolic states is difficult in humans but feasible in mice. To explore whether metabolic states can alter weight outcomes of SGLT2 inhibitor treatment, the impact of canagliflozin was studied comparatively in high-fat-diet-induced obese (DIO) mice and leptin-receptor-deficient db/db mice. Canagliflozin, orally administered, induced rapid reductions in glycemia and weight followed by elevated food intake in both models. The initial weight loss was rebounded in db/db mice, but progressed and sustained in DIO mice accompanied by circadian rises in body temperature and locomotor activity, the effects possibly balancing the elevated food intake. These results reveal that physical/metabolic states, independent of social/psychological factors, influence weight outcome of canagliflozin treatment.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100079"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13199774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147982258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Non-nutritive sweeteners attenuate reinforced cephalic phase insulin release and impair glucose tolerance in mice. 非营养性甜味剂可减弱小鼠头期胰岛素的增强释放并损害葡萄糖耐量。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-07-01 Epub Date: 2026-02-27 DOI: 10.1016/j.jphyss.2026.100066
Tomonari Otsuki, Keiji Okihara, Kengo Nomura, Sho Matsui, Akiyuki Taruno, Tsutomu Sasaki
{"title":"Non-nutritive sweeteners attenuate reinforced cephalic phase insulin release and impair glucose tolerance in mice.","authors":"Tomonari Otsuki, Keiji Okihara, Kengo Nomura, Sho Matsui, Akiyuki Taruno, Tsutomu Sasaki","doi":"10.1016/j.jphyss.2026.100066","DOIUrl":"10.1016/j.jphyss.2026.100066","url":null,"abstract":"<p><p>Non-nutritive artificial sweeteners (NNSs) which provide sweetness with minimal calories are used to reduce sugar consumption, while orosensory stimuli such as sweet taste can stimulate insulin secretion known as cephalic phase insulin release (CPIR). Whether the use of NNSs affects CPIR and glucose homeostasis remains unclear. Here, we report that NNSs impair CPIR reinforced by glucose solution conditioning and disturb glucose homeostasis in mice without affecting peripheral sensing of the tastant through the chorda tympani nerve. We established a protocol for reinforcing CPIR and detecting it in male C57BL/6 mice. Consumption of the NNSs for 2 days impaired the reinforced CPIR and the improved glucose tolerance by the consumption of 1 M glucose solution. These results suggest that NNS impairs glucose tolerance partly by disturbing CPIR in mice.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 2","pages":"100066"},"PeriodicalIF":3.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12969289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of serotonin transporters on myocardial cell injury during ischemia/reperfusion in rats. 血清素转运体对大鼠缺血再灌注心肌细胞损伤的影响。
IF 3.3 4区 医学
Journal of Physiological Sciences Pub Date : 2026-06-30 DOI: 10.1016/j.jphyss.2026.100085
Yoshimasa Kishi, Shuji Shimizu, Yosuke Kuroko, Yasuhiro Kotani, Tsuyoshi Akiyama, Shingo Kasahara
{"title":"Effects of serotonin transporters on myocardial cell injury during ischemia/reperfusion in rats.","authors":"Yoshimasa Kishi, Shuji Shimizu, Yosuke Kuroko, Yasuhiro Kotani, Tsuyoshi Akiyama, Shingo Kasahara","doi":"10.1016/j.jphyss.2026.100085","DOIUrl":"10.1016/j.jphyss.2026.100085","url":null,"abstract":"<p><p>Serotonin (5-HT) reuptake in the heart is mediated by the platelet serotonin reuptake transporter (SERT) and the cardiomyocyte plasma membrane monoamine transporter (PMAT). However, the specific roles of these transporters in myocardial cell injury during ischemia/reperfusion remain unclear. Sprague-Dawley rats underwent left coronary artery occlusion followed by reperfusion. Using cardiac microdialysis technique, fluoxetine (SERT inhibitor, 900 μM) or decynium 22 (PMAT inhibitor, 100 μM) was administered locally to the ischemic region. Myoglobin concentrations in the dialysate were measured during ischemia followed by reperfusion. In the fluoxetine-treated group, peak myoglobin concentration (14,889 ± 1364 ng/mL) during 0-15 min of reperfusion was significantly higher compared to both the control group (9800 ± 1627 ng/mL) and the decynium 22-treated group (8172 ± 877 ng/mL) (P < 0.01 for both). Local SERT inhibition exacerbated myocardial cell injury during ischemia/reperfusion. However, co-inhibition of PMAT reduced myocardial cell injury under SERT inhibition to the control level.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"76 3","pages":"100085"},"PeriodicalIF":3.3,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148382208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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