Summary
Potassium transporters and channels play crucial roles in K+ uptake and translocation in plant cells. These roles are essential for plant growth and development. AKT1 is an important K+ ...channel in Arabidopsis roots that is involved in K+ uptake. It is known that AKT1 is activated by a protein kinase CIPK23 interacting with two calcineurin B‐like proteins CBL1/CBL9. The present study showed that another calcineurin B‐like protein (CBL10) may also regulate AKT1 activity. The CBL10‐over‐expressing lines showed a phenotype as sensitive as that of the akt1 mutant under low‐K+ conditions. In addition, the K+ content of both CBL10‐over‐expressing lines and akt1 mutant plants were significantly reduced compared with wild‐type plants. Moreover, CBL10 directly interacted with AKT1, as verified in yeast two‐hybrid, BiFC and co‐immunoprecipitation experiments. The results of electrophysiological analysis in both Xenopus oocytes and Arabidopsis root cell protoplasts demonstrated that CBL10 impairs AKT1‐mediated inward K+ currents. Furthermore, the results from the yeast two‐hybrid competition assay indicated that CBL10 may compete with CIPK23 for binding to AKT1 and negatively modulate AKT1 activity. The present study revealed a CBL‐interacting protein kinase‐independent regulatory mechanism of calcineurin B‐like proteins in which CBL10 directly regulates AKT1 activity and affects ion homeostasis in plant cells.
Potassium and nitrogen are essential mineral elements for plant growth and development. The protein kinase LKS1/CIPK23 is involved in both K+ and NH4+ uptake in Arabidopsis root. The transcripts of ...LKS1 can be induced by low K+ (0.1 mM) and high NH4+ (30 mM); however, the molecular mechanism is still unknown. In this study, we isolated the transcription factor STOP1 that positively regulates LKS1 transcription in Arabidopsis responses to both low-K+ and high-NH4+ stresses. STOP1 proteins can directly bind to the LKS1 promoter, promoting its transcription. The stop1 mutants displayed a leaf chlorosis phenotype similar to lks1 mutant when grown on low-K+ and high-NH4+ medium. On the other hand, STOP1 overexpressing plants exhibited a similar tolerant phenotype to LKS1 overexpressing plants. The transcript level of STOP1 was only upregulated by low K+ rather than high NH4+; however, the accumulation of STOP1 protein in the nucleus was required for the upregulation of LKS1 transcripts in both low-K+ and high-NH4+ responses. Our data demonstrate that STOP1 positively regulates LKS1 transcription under low-K+ and high-NH4+ conditions; therefore, LKS1 promotes K+ uptake and inhibits NH4+ uptake. The STOP1/LKS1 pathway plays crucial roles in K+ and NH4+ homeostasis, which coordinates potassium and nitrogen balance in plants in response to external fluctuating nutrient levels.
Potassium (K
) is one of essential mineral elements for plant growth and development. K
channels, especially AKT1-like channels, play crucial roles in K
uptake in plant roots. Maize is one of ...important crops; however, the K
uptake mechanism in maize is little known. Here, we report the physiological functions of K
channel ZMK1 in K
uptake and homeostasis in maize.
is a homolog of
channel in maize, and mainly expressed in maize root. Yeast complementation experiments and electrophysiological characterization in
oocytes indicated that ZMK1 could mediate K
uptake.
rescued the low-K
-sensitive phenotype of
mutant and enhanced K
uptake in
. Overexpression of
also significantly increased K
uptake activity in maize, but led to an oversensitive phenotype. Similar to AKT1 regulation, the protein kinase ZmCIPK23 interacted with ZMK1 and phosphorylated the cytosolic region of ZMK1, activating ZMK1-mediated K
uptake.
could also complement the low-K
-sensitive phenotype of
/
mutant. These findings demonstrate that ZMK1 together with ZmCIPK23 plays important roles in K
uptake and homeostasis in maize.
Delivery of exogenous high mobility group box 1 (HMGB1) may exert a beneficial effect on myocardial ischemia-reperfusion (I/R) injury. Since the expression of vascular endothelial growth factor ...(VEGF) and phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) in the myocardium mediates the cardioprotective function of basic fibroblast growth factor, we hypothesized that VEGF and the PI3K/Akt signaling pathway also mediate the protective effects of intravenously delivered HMGB1. Thus, the objective of the present study was to analyze the impact of intravenous administration of HMGB1 on the myocardial expression of VEGF, myocardial fibrosis, and cardiac function in rats subjected to acute myocardial I/R. The ischemia was induced by ligation of the left anterior descending coronary artery for 30 min and was followed by 3 h of reperfusion. Myocardial malondialdehyde content, infarct size, and collagen volume fraction decreased, while the activity of superoxide dismutase was increased, the expression of VEGF and p-Akt was upregulated, and cardiac function was improved in the HMGB1-treated group when compared with rats subjected to I/R only (all
< 0.05). However, these effects of HMGB1 were abolished by LY294002. The obtained results demonstrate that the cardioprotective effects of intravenous administration of HMGB1 prior to I/R may be mediated by upregulation of myocardial expression of VEGF, which may activate the PI3K/Akt signaling pathway.
This study aimed to explore the prognostic value of leukocyte telomere length (LTL) in patients with coronary artery disease (CAD).
We enrolled 366 CAD patients and 76 healthy subjects in this study. ...LTL was measured. All subjects were followed up for 6 months for further analysis regarding major adverse cardiac events (MACEs).
CAD patients had a significantly shortened LTL compared with healthy subjects (p < 0.05). The area under the curve for LTL prediction of MACEs was 0.769 (p < 0.001), with a shorter LTL being an independent predictor of MACEs (Cox proportional hazards regression, hazard ratio: 2.866; p < 0.001).
LTL could be considered as an independent predictor of short-term MACEs in CAD.
The present study aimed to determine the effects of high mobility group box 1 protein (HMGB1) on myocardial ischemia reperfusion (I/R) injury in rats following acute myocardial ischemia and ...investigate the underlying molecular mechanisms of these effects. Male Wistar rats were randomly divided into the following groups (n=10/group): Sham operation; I/R; HMGB50 (50 ng/kg HMGB1 before I/R); HMGB100 (100 ng/kg HMGB1 before I/R); and HMGB200 (200 ng/kg HMGB1 before I/R). Serum cardiac troponin I (cTnI), interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels were subsequently measured. Myocardial levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were also determined. Myocardial infarction size (IS) was determined by 2,3,5-triphenyltetrazolium chloride staining. Myocardial expression of hypoxia inducible factor (HIF)-1α and phosphorylated p38 mitogen-activated protein kinase (P-p38 MAPK) protein was measured using western blotting. The results demonstrated that HMGB1 significantly decreased serum levels of cTnI, IL-6 and TNF-α and myocardial IS in I/R rats compared with the sham group (all P<0.05). HMGB1 also significantly decreased and increased myocardial levels of MDA and SOD, respectively (both P<0.05). HMGB1 significantly increased myocardial expression of HIF-1α and decreased expression of P-p38 MAPK following I/R (both P<0.05). These effects of HMGB1 occurred in a dose-dependent manner. The results of the current study indicate that the cardioprotective effects of intravenous HMGB1 are associated with increased myocardial expression of HIF-1α via inhibition of P-p38 MAPK expression, leading to inhibition of the P-p38 MAPK signaling pathway.
Objective To investigate the effect of basic fibroblast growth factor (bFGF) on myocardial expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) following ...acute myocardial infarction (AMI) in rats. Methods Eighty male Sprague-Dawley rats were divided into sham operation ( n = 20), AMI control ( n = 20), bFGF50 (intravenous bFGF 50 μg/kg/d, n = 20) and bFGF200 (intravenous bFGF 200 μg/kg/d, n = 20) groups. The left ventricular ejection fraction (LVEF) was measured by echocardiography. The expression of HIF-1α mRNA and VEGF mRNA in the ischaemic tissues was analysed by reverse transcription-polymerase chain reaction. Results The LVEF in the bFGF50 and bFGF200 group was higher than in the AMI control group ( p < 0.05) seven and 14 days after the treatment. There was no difference in HIF-1α mRNA expression between the bFGF50 and AMI control group ( p > 0.05). However, the HIF-1α mRNA expression in the bFGF200 group was higher than in the AMI control group seven days (1.13 ± 0.18 vs 0.90 ± 0.14, p < 0.01) and 14 days (1.31 ± 0.18 vs 0.93 ± 0.09, p < 0.01) after the treatment. The VEGF mRNA expression in the bFGF200 group was also higher than in the AMI control group seven days (1.10 ± 0.17 vs 0.86 ± 0.14, p < 0.01) and 14 days after the AMI (1.28 ± 0.19 vs 0.89 ± 0.14, p < 0.01). Conclusions bFGF therapy was associated with an improvement in left ventricular function and an increase in myocardial expression of HIF-1α mRNA and VEGF mRNA following AMI. bFGF may exert its cardioprotective effect through upregulating HIF-1α mRNA and VEGF mRNA in the ischaemic myocardium.
PDF
