Alterations in cellular calcium(Ca^(2+))signals have been causally associated with the development and progression of human cancers.Cellular Ca^(2+)signals are generated by channels,pumps,and exchangers that move Ca^(...Alterations in cellular calcium(Ca^(2+))signals have been causally associated with the development and progression of human cancers.Cellular Ca^(2+)signals are generated by channels,pumps,and exchangers that move Ca^(2+)ions across membranes and are decoded by effector proteins in the cytosol or in organelles.S-acylation,the reversible addition of 16-carbon fatty acids to proteins,modulates the activity of Ca^(2+)transporters by altering their affinity for lipids,and enzymes mediating this reversible post-translational modification have also been linked to several types of cancers.Here,we compile studies reporting an association between Ca^(2+)transporters or S-acylation enzymes with specific cancers,as well as studies reporting or predicting the S-acylation of Ca^(2+)transporters.We then discuss the potential role of S-acylation in the oncogenic potential of a subset of Ca^(2+)transport proteins involved in cancer.展开更多
Ca^(2+) signaling is critical for heart development;however,the precise roles and regulatory pathways of Ca^(2+) transport proteins in cardiogenesis remain largely unknown.Sodium-calcium exchanger 1(Ncx1)is responsibl...Ca^(2+) signaling is critical for heart development;however,the precise roles and regulatory pathways of Ca^(2+) transport proteins in cardiogenesis remain largely unknown.Sodium-calcium exchanger 1(Ncx1)is responsible for Ca^(2+) efflux in cardiomyocytes.It is involved in cardiogenesis,while the mechanism is unclear.Here,using the forward genetic screening in zebrafish,we identified a novel mutation at a highly-conserved leucine residue in ncx1 gene(mutant^(LDD353)/ncx1h^(L154P))that led to smaller hearts with reduced heart rate and weak contraction.Mechanistically,the number of ventricular but not atrial cardiomyocytes was reduced in ncx1h^(L154P) zebrafish.These defects were mimicked by knockdown or knockout of ncx1h.Moreover,ncx1h^(L154P) had cytosolic and mitochondrial Ca^(2+) overloading and Ca^(2+) transient suppression in cardiomyocytes.Furthermore,ncx1h^(L154P) and ncx1h morphants downregulated cardiac transcription factors hand2 and gata4 in the cardiac regions,while overexpression of hand2 and gata4 partially rescued cardiac defects including the number of ventricular myocytes.These findings demonstrate an essential role of the novel 154th leucine residue in the maintenance of Ncx1 function in zebrafish,and reveal previous unrecognized critical roles of the 154th leucine residue and Ncx1 in the formation of ventricular cardiomyocytes by at least partially regulating the expression levels of gata4 and hand2.展开更多
On the basis of two types of calcium transport system detected in the barley root plasma membrane,the mechanisms of the calcium transport have been further studied.Ionophore CCCP has been found to inhibit Mg^(2+) -dep...On the basis of two types of calcium transport system detected in the barley root plasma membrane,the mechanisms of the calcium transport have been further studied.Ionophore CCCP has been found to inhibit Mg^(2+) -dependent calcium transport by 20%.In contrast,Mg^(2+) -independent calcium trans- port is insensitive to CCCP.The Mg^(2+) -dependent calcium transport following the collapse of H^+ gradient across the plasma membrane could be driven by the H^+ gradient either set up by ATP or imposed artificially. Any relation between Mg^(2+) -independent calcium transport and H^+ gradient has not been observed.These results indicate that Mg^(2+) -dependent calcium transport is accompanied by the decrease of H^+ gradient,and Mg^(2+) -independent calcium transport has nothing to do with the H^+ gradient.It is therefore suggested that the calcium transport across the barley root plasma membrane is driven by ATPase that is independent of Mg^(2+),and H^+/Ca^(2+) antiporter that is dependent on Mg^(2+).展开更多
Plant mineral nutrition is essential for crop yields and human health.However,the uneven distribution of mineral elements over time and space leads to a lack or excess of available mineral elements in plants.Among the...Plant mineral nutrition is essential for crop yields and human health.However,the uneven distribution of mineral elements over time and space leads to a lack or excess of available mineral elements in plants.Among the essential nutrients,calcium(Ca^(2+))stands out as a prominent second messenger that plays crucial roles in response to extracellular stimuli in all eukaryotes.Distinct Ca^(2+)signatures with unique parameters are induced by different stresses and deciphered by various Ca^(2+)sensors.Recent research on the participation of Ca^(2+)signaling in regulation of mineral elements has made great progress.In this review,we focus on the impact of Ca^(2+)signaling on plant mineral uptake and detoxification.Specifically,we emphasize the significance of Ca^(2+)signaling for regulation of plant mineral nutrition and delve into key points and novel avenues for future investigations,aiming to offer new insights into plant ion homeostasis.展开更多
The relationship between mitochondrial Ca2+ transport and permeability transition pore (PTP) opening as well as the effects of mitochondrial energetic status on mitochondrial Ca2+ transport and PTP opening were studie...The relationship between mitochondrial Ca2+ transport and permeability transition pore (PTP) opening as well as the effects of mitochondrial energetic status on mitochondrial Ca2+ transport and PTP opening were studied. The results showed that the calcium-induced calcium release from mitochondria (mClCR) induced PTP opening. Inhibitors for electron transport of respiratory chain inhibited mClCR and PTP opening. Partial recovery of electron transport in respiratory chain resulted in partial recovery of mClCR and PTP opening. mClCR and PTP opening were also inhibited by CCCP which eliminated transmembrane proton gradient. The results indicated that mitochondrial Ca2+ transport and PTP opening are largely dependent on electron transport and energy coupling.展开更多
Objective:To investigate the regulatory effect of Qiliqiangxin Capsule on mitochondrial Ca^(2+)related genes in rats with myocardial infarction(MI).Methods:The rat model of MI was established by ligation of the left a...Objective:To investigate the regulatory effect of Qiliqiangxin Capsule on mitochondrial Ca^(2+)related genes in rats with myocardial infarction(MI).Methods:The rat model of MI was established by ligation of the left anterior descending coronary artery.After operation,the rats were randomly assigned to the model group,the Qiliqiangxin group and the captopril group;a sham-operated group was also available as a control.After four weeks of treatment,the extent of infarction in rats was observed by gross cardiac structure and the morphological changes of myocardial histopathology were observed by HE staining.Detection of mitochondrial Ca^(2+)transport-related genes such as inositol-1,4,5-trisphosphate receptor 2(IP3R2),glucose regulated protein 75(GRP75),voltage-dependent anion channel 1(VDAC1),and mitofusion 2(Mfn2)and mitochondrial apoptosis-related genes such as B-cell lymphoma-2(Bcl-2)and Bcl-2 related X protein(Bax)mRNA expression changes was measured by RT-PCR in the infarct margins of the heart;Western blot was used to detect changes in Bcl-2,Bax protein expression in myocardial tissue.The rate of apoptosis in cardiac myocardial tissue was detected by TUNEL staining.Results:Compared with the sham group,the anterior left ventricular wall of the model group showed a large area of infarction,and the structure of myocardial tissue was disordered.The mRNA expression level of mitochondrial Ca^(2+)transport-related genes such as IP3R2,GRP75,VDAC1,and Mfn2 were significantly increased(P<0.05,P<0.01);The mRNA and protein expression of Bcl-2,a molecule related to mitochondrial apoptosis,were significantly decreased(P<0.01),while the mRNA and protein expression of Bax were significantly increased(P<0.01);and apoptosis rate was significantly increased(P<0.01).Compared with the model group,the infarct size of cardiac gross specimens in the Qiliqiangxin group and the captopril group was reduced and myocardial fibers were relatively well ordered;The mRNA expression of mitochondrial Ca^(2+)transport-related genes such as IP3R2展开更多
This paper studied the changes of SR Ca2+transport capacity of different skeletal muscle fiber types in rats immediately after they ran on a motor-driven treadmill at 18 m/min （100 mins）. The results showed that SR ...This paper studied the changes of SR Ca2+transport capacity of different skeletal muscle fiber types in rats immediately after they ran on a motor-driven treadmill at 18 m/min （100 mins）. The results showed that SR Ca2+-ATPase activity of slow-twitch and fast-twitch fibers decreased by 83. 32% （P＞0.01） and 12．18％ （P＜0. 05） respectively in comparison with the values of control group. Moreover,there were obvious reductions in both the iultial rate of SR Ca2+ uptake and .the maximal capacity of SR Ca2+ uptake in slow -twitch fibers after running. These findings suggested that the decreases of the SR Ca2+ transport capacity of different muscle fiber types might be related to the exertise-induced fatigue of skeletal muscles.展开更多
基金Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung(Grant/Award Number:310030_189042)。
文摘Alterations in cellular calcium(Ca^(2+))signals have been causally associated with the development and progression of human cancers.Cellular Ca^(2+)signals are generated by channels,pumps,and exchangers that move Ca^(2+)ions across membranes and are decoded by effector proteins in the cytosol or in organelles.S-acylation,the reversible addition of 16-carbon fatty acids to proteins,modulates the activity of Ca^(2+)transporters by altering their affinity for lipids,and enzymes mediating this reversible post-translational modification have also been linked to several types of cancers.Here,we compile studies reporting an association between Ca^(2+)transporters or S-acylation enzymes with specific cancers,as well as studies reporting or predicting the S-acylation of Ca^(2+)transporters.We then discuss the potential role of S-acylation in the oncogenic potential of a subset of Ca^(2+)transport proteins involved in cancer.
基金supported by grants from the National Natural Science Foundation of China(81520108004,81470422)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDA16010201)+1 种基金National Key R&D Program of China(2017YFA 0103700,2016YFC1301204)to H.-T.Y.Shanghai Natural Science Foundation(17ZR1435500)to J.H。
文摘Ca^(2+) signaling is critical for heart development;however,the precise roles and regulatory pathways of Ca^(2+) transport proteins in cardiogenesis remain largely unknown.Sodium-calcium exchanger 1(Ncx1)is responsible for Ca^(2+) efflux in cardiomyocytes.It is involved in cardiogenesis,while the mechanism is unclear.Here,using the forward genetic screening in zebrafish,we identified a novel mutation at a highly-conserved leucine residue in ncx1 gene(mutant^(LDD353)/ncx1h^(L154P))that led to smaller hearts with reduced heart rate and weak contraction.Mechanistically,the number of ventricular but not atrial cardiomyocytes was reduced in ncx1h^(L154P) zebrafish.These defects were mimicked by knockdown or knockout of ncx1h.Moreover,ncx1h^(L154P) had cytosolic and mitochondrial Ca^(2+) overloading and Ca^(2+) transient suppression in cardiomyocytes.Furthermore,ncx1h^(L154P) and ncx1h morphants downregulated cardiac transcription factors hand2 and gata4 in the cardiac regions,while overexpression of hand2 and gata4 partially rescued cardiac defects including the number of ventricular myocytes.These findings demonstrate an essential role of the novel 154th leucine residue in the maintenance of Ncx1 function in zebrafish,and reveal previous unrecognized critical roles of the 154th leucine residue and Ncx1 in the formation of ventricular cardiomyocytes by at least partially regulating the expression levels of gata4 and hand2.
文摘On the basis of two types of calcium transport system detected in the barley root plasma membrane,the mechanisms of the calcium transport have been further studied.Ionophore CCCP has been found to inhibit Mg^(2+) -dependent calcium transport by 20%.In contrast,Mg^(2+) -independent calcium trans- port is insensitive to CCCP.The Mg^(2+) -dependent calcium transport following the collapse of H^+ gradient across the plasma membrane could be driven by the H^+ gradient either set up by ATP or imposed artificially. Any relation between Mg^(2+) -independent calcium transport and H^+ gradient has not been observed.These results indicate that Mg^(2+) -dependent calcium transport is accompanied by the decrease of H^+ gradient,and Mg^(2+) -independent calcium transport has nothing to do with the H^+ gradient.It is therefore suggested that the calcium transport across the barley root plasma membrane is driven by ATPase that is independent of Mg^(2+),and H^+/Ca^(2+) antiporter that is dependent on Mg^(2+).
基金supported by the National Natural Science Foundation of China(32222008 to C.W.)the China Postdoctoral Science Foundation(2023M732883 to C.J.).
文摘Plant mineral nutrition is essential for crop yields and human health.However,the uneven distribution of mineral elements over time and space leads to a lack or excess of available mineral elements in plants.Among the essential nutrients,calcium(Ca^(2+))stands out as a prominent second messenger that plays crucial roles in response to extracellular stimuli in all eukaryotes.Distinct Ca^(2+)signatures with unique parameters are induced by different stresses and deciphered by various Ca^(2+)sensors.Recent research on the participation of Ca^(2+)signaling in regulation of mineral elements has made great progress.In this review,we focus on the impact of Ca^(2+)signaling on plant mineral uptake and detoxification.Specifically,we emphasize the significance of Ca^(2+)signaling for regulation of plant mineral nutrition and delve into key points and novel avenues for future investigations,aiming to offer new insights into plant ion homeostasis.
文摘The relationship between mitochondrial Ca2+ transport and permeability transition pore (PTP) opening as well as the effects of mitochondrial energetic status on mitochondrial Ca2+ transport and PTP opening were studied. The results showed that the calcium-induced calcium release from mitochondria (mClCR) induced PTP opening. Inhibitors for electron transport of respiratory chain inhibited mClCR and PTP opening. Partial recovery of electron transport in respiratory chain resulted in partial recovery of mClCR and PTP opening. mClCR and PTP opening were also inhibited by CCCP which eliminated transmembrane proton gradient. The results indicated that mitochondrial Ca2+ transport and PTP opening are largely dependent on electron transport and energy coupling.
基金This study was supported by Beijing University of Traditional Chinese Medicine Dongzhimen Hospital 2022 Science and Technology Innovation Special Project(DZMKJCX-2022-008)。
文摘Objective:To investigate the regulatory effect of Qiliqiangxin Capsule on mitochondrial Ca^(2+)related genes in rats with myocardial infarction(MI).Methods:The rat model of MI was established by ligation of the left anterior descending coronary artery.After operation,the rats were randomly assigned to the model group,the Qiliqiangxin group and the captopril group;a sham-operated group was also available as a control.After four weeks of treatment,the extent of infarction in rats was observed by gross cardiac structure and the morphological changes of myocardial histopathology were observed by HE staining.Detection of mitochondrial Ca^(2+)transport-related genes such as inositol-1,4,5-trisphosphate receptor 2(IP3R2),glucose regulated protein 75(GRP75),voltage-dependent anion channel 1(VDAC1),and mitofusion 2(Mfn2)and mitochondrial apoptosis-related genes such as B-cell lymphoma-2(Bcl-2)and Bcl-2 related X protein(Bax)mRNA expression changes was measured by RT-PCR in the infarct margins of the heart;Western blot was used to detect changes in Bcl-2,Bax protein expression in myocardial tissue.The rate of apoptosis in cardiac myocardial tissue was detected by TUNEL staining.Results:Compared with the sham group,the anterior left ventricular wall of the model group showed a large area of infarction,and the structure of myocardial tissue was disordered.The mRNA expression level of mitochondrial Ca^(2+)transport-related genes such as IP3R2,GRP75,VDAC1,and Mfn2 were significantly increased(P<0.05,P<0.01);The mRNA and protein expression of Bcl-2,a molecule related to mitochondrial apoptosis,were significantly decreased(P<0.01),while the mRNA and protein expression of Bax were significantly increased(P<0.01);and apoptosis rate was significantly increased(P<0.01).Compared with the model group,the infarct size of cardiac gross specimens in the Qiliqiangxin group and the captopril group was reduced and myocardial fibers were relatively well ordered;The mRNA expression of mitochondrial Ca^(2+)transport-related genes such as IP3R2
文摘This paper studied the changes of SR Ca2+transport capacity of different skeletal muscle fiber types in rats immediately after they ran on a motor-driven treadmill at 18 m/min （100 mins）. The results showed that SR Ca2+-ATPase activity of slow-twitch and fast-twitch fibers decreased by 83. 32% （P＞0.01） and 12．18％ （P＜0. 05） respectively in comparison with the values of control group. Moreover,there were obvious reductions in both the iultial rate of SR Ca2+ uptake and .the maximal capacity of SR Ca2+ uptake in slow -twitch fibers after running. These findings suggested that the decreases of the SR Ca2+ transport capacity of different muscle fiber types might be related to the exertise-induced fatigue of skeletal muscles.
