Serum response factor(SRF) is a transcription factor that regulates many genes involved in cellular activities such as proliferation,migration,differentiation,angiogenesis,and apoptosis.Although it has only been known...Serum response factor(SRF) is a transcription factor that regulates many genes involved in cellular activities such as proliferation,migration,differentiation,angiogenesis,and apoptosis.Although it has only been known for about two decades,SRF has been studied extensively.To date,over a thousand SRF studies have been published,but it still remains a hot topic.Due to its critical role in mesoderm-derived tissues,most of the SRF studies focused on muscle structure/function,cardiovascular development/maintenance,and smooth muscle generation/repair.Recently,SRF has received more attention in the digestive field and several important discoveries have been made.This review will summarize what we have learned about SRF in the gastrointestinal tract and provide insights into possible future directions in this area.展开更多
Studies have snown that serum response factor is beneficaial for axonar regeneration of peripheral herves.However,Its role after central nervous system injury remains unclear. In this study,we established a rat model ...Studies have snown that serum response factor is beneficaial for axonar regeneration of peripheral herves.However,Its role after central nervous system injury remains unclear. In this study,we established a rat model of T9-T10 spinal cord transection injury.We found that the expression of serum response factor in injured spinal cord gray matter neurons gradually increased with time,reached its peak on the 7^(th) day,and then gradually decreased.To investigate the role of serum response factor,we used lentivirus vecto rs to ove rexpress and silence serum response factor in spinal cord tissue.We found that overexpression of serum response factor promoted motor function recovery in rats with spinal cord injury.Qualitative observation of biotinylated dextran amine anterograde tra cing showed that ove rexpression of serum response factor increased nerve fibers in the injured spinal co rd.Additionally,transmission electron microscopy showed that axon and myelin sheath morphology was restored.Silencing serum response factor had the opposite effects of ove rexpression.These findings suggest that serum response factor plays a role in the recovery of motor function after spinal cord injury.The underlying mechanism may be related to the regulation of axonal regeneration.展开更多
Objective To investigate the relationship between transcription factor and the change of protein expression levels in heart failure.Methods Bioinformatic method was used to analyze the data of binding-sites on the 5&#...Objective To investigate the relationship between transcription factor and the change of protein expression levels in heart failure.Methods Bioinformatic method was used to analyze the data of binding-sites on the 5'flaking regions of four genes whose mRNA level changed in failing heart from three databases about nucleic acid-EMBL,transcriptional regulation factor-TRANSFAC and protein-SWISS-PORT.The expression level of selected transcription factor was determined by immunohischemical method.Results Nine transcription factors were inferred to influence the proteins'levels in occurrence and development of heart failure.Serum response factor(SRF)was selected from the nine factors and assayed.The results showed that there was a higher level of SRF in healthy group than in chronic heart failure(CHF),and the level was associated with the degree of CHF.It was also found that there was a relative higher level of SRF in the acute myocardial infarction(AMI)than that in CHF,but which was lower than the healthy.Conclusion It showed that SRF had a quantitative change in the development of heart failure,and suggested SRF might play an important regulative role in heart failure.The expression changes of proteins related to myocardial function might be regulated by the quantitative change of transcription factor(s).展开更多
Hypoglycemia is a frequent and potentially severe complication that can result in significant brain injury in individuals with diabetes treated with insulin or other hypoglycemic agents and in those undergoing prolong...Hypoglycemia is a frequent and potentially severe complication that can result in significant brain injury in individuals with diabetes treated with insulin or other hypoglycemic agents and in those undergoing prolonged fasting.Despite its clinical importance,the molecular mechanisms through which hypoglycemia induces neurodegeneration remain poorly defined.We therefore investigated the molecular and cellular basis of hypoglycemia-induced brain damage using human neuron and glial cell cultures in vitro and hypoglycemic mouse models in vivo.We found that starvation-induced hypoglycemia triggers hallmark neurodegenerative features,such as astrocyte activation and microglial reactivity,that closely resemble those found in the brains of hypoglycemic mouse models.Neurons notably activate an adaptive survival response mediated by serum response factor(SRF)and myocardin-related transcription factor-A(MRTF-A),which drives a metabolic reprogramming process.This shift enables neurons to use extracellular matrix components as alternative energy sources under glucose deprivation.However,this compensatory mechanism results in the excessive accumulation of urea cycle byproducts,which subsequently exacerbates neuronal damage and promotes glial activation.Glucose refeeding remarkably reversed these neurodegenerative features by deactivating SRF/MRTF-A signaling in both in vitro and in vivo.Collectively,our results revealed a neuron-intrinsic mechanism linking glucose deprivation to reversible neurodegeneration via SRF/MRTF-A,offering potential targets for preventing hypoglycemia-associated brain damage.展开更多
The water-soluble conjugated polyelectrolyte, poly[3-（1′-ethyloxy-2′-N- methylimidazole）thiophene]（PEOIMT）, was prepared. Its photophysical and electrochemical properties, and response characteristics to the ext...The water-soluble conjugated polyelectrolyte, poly[3-（1′-ethyloxy-2′-N- methylimidazole）thiophene]（PEOIMT）, was prepared. Its photophysical and electrochemical properties, and response characteristics to the external condition（e g, temperature response, solvent response and pH response）, were investigated. The results show the PEOIMT belongs to the organic semiconductor. The interaction between the PEOIMT and the bovine serum albumin（BSA） was investigated using UV-vis spectroscopy. It was found that the PEOIMT could interact with the BSA. The PEOIMT can be used as a biosensor to detect the BSA.展开更多
Purpose： Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgra...Purpose： Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgravity （SMG）. Methods： We utilized the rotary cell culture system （RCCS-1） to explore the subsequent effects of SMG on human umbilical vein endothelial cells （HUVECs）. Results： SMG-treated HUVECs appeared obvious growth inhibition after return to normal gravity, which might be attributed to a set of responses including alteration of cytoskeleton, decreased cell adhesion capacity and increased apoptosis. Expression levels of mTOR and its downstream Apaf-1 were increased during subsequent culturing after SMG. miR-22 was up-regulated and its target genes SRF and LAMC1 were down-regulated at mRNA levels. LAMC1 siRNAs reduced cell adhesion rate and inhibited stress fiber formation while SRF siRNAs caused apoptosis. Conclusion： SMG has the subsequent biological effects on HUVECs, resulting in growth inhibition through mTOR signaling and miR-22-mediated mechanism.展开更多
基金Supported by The Department of Veterans Affairs of the United States and the American Heart Association grants to Dr Chai J
文摘Serum response factor(SRF) is a transcription factor that regulates many genes involved in cellular activities such as proliferation,migration,differentiation,angiogenesis,and apoptosis.Although it has only been known for about two decades,SRF has been studied extensively.To date,over a thousand SRF studies have been published,but it still remains a hot topic.Due to its critical role in mesoderm-derived tissues,most of the SRF studies focused on muscle structure/function,cardiovascular development/maintenance,and smooth muscle generation/repair.Recently,SRF has received more attention in the digestive field and several important discoveries have been made.This review will summarize what we have learned about SRF in the gastrointestinal tract and provide insights into possible future directions in this area.
基金supported by the National Natural Science Foundation of China,No.81 8 70985 (to FH)Project of Shandong Province Higher Education Science and Technology Program,No.J18KA258 (to NLZ)+1 种基金Xu Rongxiang Regenerative Medicine Science and Technology Program of Binzhou Medical University,No.BY2020XRX06 (to NLZ)the Natural Science Foundation of Shandong Province,No.BS2015SW021 (to NLZ)。
文摘Studies have snown that serum response factor is beneficaial for axonar regeneration of peripheral herves.However,Its role after central nervous system injury remains unclear. In this study,we established a rat model of T9-T10 spinal cord transection injury.We found that the expression of serum response factor in injured spinal cord gray matter neurons gradually increased with time,reached its peak on the 7^(th) day,and then gradually decreased.To investigate the role of serum response factor,we used lentivirus vecto rs to ove rexpress and silence serum response factor in spinal cord tissue.We found that overexpression of serum response factor promoted motor function recovery in rats with spinal cord injury.Qualitative observation of biotinylated dextran amine anterograde tra cing showed that ove rexpression of serum response factor increased nerve fibers in the injured spinal co rd.Additionally,transmission electron microscopy showed that axon and myelin sheath morphology was restored.Silencing serum response factor had the opposite effects of ove rexpression.These findings suggest that serum response factor plays a role in the recovery of motor function after spinal cord injury.The underlying mechanism may be related to the regulation of axonal regeneration.
基金This work was supported by the National Natural Science Foundation of China(No.30300130).
文摘Objective To investigate the relationship between transcription factor and the change of protein expression levels in heart failure.Methods Bioinformatic method was used to analyze the data of binding-sites on the 5'flaking regions of four genes whose mRNA level changed in failing heart from three databases about nucleic acid-EMBL,transcriptional regulation factor-TRANSFAC and protein-SWISS-PORT.The expression level of selected transcription factor was determined by immunohischemical method.Results Nine transcription factors were inferred to influence the proteins'levels in occurrence and development of heart failure.Serum response factor(SRF)was selected from the nine factors and assayed.The results showed that there was a higher level of SRF in healthy group than in chronic heart failure(CHF),and the level was associated with the degree of CHF.It was also found that there was a relative higher level of SRF in the acute myocardial infarction(AMI)than that in CHF,but which was lower than the healthy.Conclusion It showed that SRF had a quantitative change in the development of heart failure,and suggested SRF might play an important regulative role in heart failure.The expression changes of proteins related to myocardial function might be regulated by the quantitative change of transcription factor(s).
基金supported by the National Research Foundation of Korea(NRF)grants funded by the Korean Government(MSIT)(RS-2021-NR061841,RS-2024-00424551,RS-2024-00395393,and RS-2024-00346657)Korea Institute of Radiological and Medical Sciences(50531-2025)KIST Institutional Program(2E33712).
文摘Hypoglycemia is a frequent and potentially severe complication that can result in significant brain injury in individuals with diabetes treated with insulin or other hypoglycemic agents and in those undergoing prolonged fasting.Despite its clinical importance,the molecular mechanisms through which hypoglycemia induces neurodegeneration remain poorly defined.We therefore investigated the molecular and cellular basis of hypoglycemia-induced brain damage using human neuron and glial cell cultures in vitro and hypoglycemic mouse models in vivo.We found that starvation-induced hypoglycemia triggers hallmark neurodegenerative features,such as astrocyte activation and microglial reactivity,that closely resemble those found in the brains of hypoglycemic mouse models.Neurons notably activate an adaptive survival response mediated by serum response factor(SRF)and myocardin-related transcription factor-A(MRTF-A),which drives a metabolic reprogramming process.This shift enables neurons to use extracellular matrix components as alternative energy sources under glucose deprivation.However,this compensatory mechanism results in the excessive accumulation of urea cycle byproducts,which subsequently exacerbates neuronal damage and promotes glial activation.Glucose refeeding remarkably reversed these neurodegenerative features by deactivating SRF/MRTF-A signaling in both in vitro and in vivo.Collectively,our results revealed a neuron-intrinsic mechanism linking glucose deprivation to reversible neurodegeneration via SRF/MRTF-A,offering potential targets for preventing hypoglycemia-associated brain damage.
基金Funded by the NationalNatural Science Foundation of China(Nos.20674022,20774031 and 21074039)the Natural Science Foundation of Guangdong province(Nos.2006A10702003,2009B090300025 and 2010A090100001)the Specialized Research Fund for the Doctoral Program of Higher Education(No.20090172110011)
文摘The water-soluble conjugated polyelectrolyte, poly[3-（1′-ethyloxy-2′-N- methylimidazole）thiophene]（PEOIMT）, was prepared. Its photophysical and electrochemical properties, and response characteristics to the external condition（e g, temperature response, solvent response and pH response）, were investigated. The results show the PEOIMT belongs to the organic semiconductor. The interaction between the PEOIMT and the bovine serum albumin（BSA） was investigated using UV-vis spectroscopy. It was found that the PEOIMT could interact with the BSA. The PEOIMT can be used as a biosensor to detect the BSA.
基金This study was supported by the ＂National Natural Science Foundation of China （No, 31270903）＂ and the Fundamental Research Funds for the Central Universities （3132016330）,
文摘Purpose： Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgravity （SMG）. Methods： We utilized the rotary cell culture system （RCCS-1） to explore the subsequent effects of SMG on human umbilical vein endothelial cells （HUVECs）. Results： SMG-treated HUVECs appeared obvious growth inhibition after return to normal gravity, which might be attributed to a set of responses including alteration of cytoskeleton, decreased cell adhesion capacity and increased apoptosis. Expression levels of mTOR and its downstream Apaf-1 were increased during subsequent culturing after SMG. miR-22 was up-regulated and its target genes SRF and LAMC1 were down-regulated at mRNA levels. LAMC1 siRNAs reduced cell adhesion rate and inhibited stress fiber formation while SRF siRNAs caused apoptosis. Conclusion： SMG has the subsequent biological effects on HUVECs, resulting in growth inhibition through mTOR signaling and miR-22-mediated mechanism.
