Background Cold is a major abiotic stress and Huanglongbing and citrus canker disease are two devastating bacterial diseases for citrus. The Ca2+-CBL-CIPK network is known to regulate different types of stress signalling in plants. How do CBL–CIPK signalling networks function in response to cold and infection by CLas or Xcc in citrus? Results Eight calcineurin B-like proteins (CBLs) and seventeen CBL-interacting protein kinases (CIPKs) were identified from the cold-tolerant satsuma mandarin ‘Guijing2501’ (Citrus. unshiu) and CLas/Xcc-sensitive sweet orange (C. sinensis). Phylogenetic analysis revealed that both CBL and CIPK family members in citrus were classified into an ancient and a recent clade according to their conserved domain characteristics and/or intron/exon structures. Genome duplication analysis suggested that both tandem and segmental duplications contributed to the amplification of the CBL and CIPK gene families in citrus under intense purifying selection, and the duplication events only existed in the recent clades. Expression comparison of the duplicated gene pairs indicated that the duplicated CBL and CIPK genes underwent functional differentiation. Further expression analysis identified that CBL1, 5, 6, and 8 and CIPK2, 8, 12, 15, 16, and 17 were significantly regulated by multiple stresses, including cold, Xcc infection and/or CLas infection, in citrus, whereas CBL2/7 and CIPK1/4/5/11/13/14 were independently highly regulated by cold and CIPK3 was uniquely responsive to Xcc infection. The combination analyses of targeted Y2H assay and expression analysis revealed that CBL6-CIPK8 was the common signalling network in response to cold and Xcc infection, while CBL6/CBL8-CIPK14 was uniquely responsive to cold in citrus. Further stable transformation and cold tolerance assay indicated that overexpression of CuCIPK16 enhanced the cold tolerance of transgenic Arabidopsis with higher POD activity and lower MDA content. Conclusions In this study, evolution, gene expression and protein‒protein interaction analyses of citrus CBLs and CIPKs were comprehensively conducted over a genome-wide range. The results will facilitate future functional characterization of individual citrus CBLs and CIPKs under specific stresses and provide clues for the clarification of cold tolerance and disease susceptibility mechanisms in corresponding citrus cultivars.
Propofol is widely used as an intravenous anesthetic in clinical practice. Previous studies have indicated that propofol induces apoptosis in neurons. Brain-derived neurotrophic factor (BDNF), a neurotrophic factor, is associated with neuronal apoptosis. BDNF-AS, a relatively conserved long non-coding RNA, can reverse the transcription of BDNF. This study aimed to investigate the involvement of BDNF-AS in propofol-induced apoptosis in HT22 cells. HT22 cells were treated with various concentrations of propofol at different time points. BDNF-AS was silenced using BDNF-AS-targeting siRNA. TrkB was antagonized by the TrkB inhibitor, ANA-12. Flow cytometry, quantitative reverse-transcription PCR, and western blotting were performed to analyze apoptosis and the expression of genes and proteins, respectively. In propofol-treated HT22 cells, BDNF-AS was upregulated, and BDNF was downregulated in a time- and dose-dependent manner. BDNF-AS downregulation mediated by siRNA mitigated apoptosis, upregulated the expression of Bcl-2, and downregulated the expression of Bax and caspase-3, 7, and 9. ANA-12 downregulated the expression of Bcl-2, upregulated the expression of Bax and caspase-3, 7, and 9, and increased apoptosis. Our study implied that inhibition of BDNF-AS can decrease propofol-induced apoptosis by activating the BDNF/TrkB pathway. Thus, the BDNF-AS-BDNF/TrkB signaling pathway may be a valuable target for treating propofol-induced neurotoxicity.
BackgroundErector spinae plane block (ESPB), as a regional anesthesia modality, is gaining interest and has been used in abdominal, thoracic and breast surgeries. The evidence on the efficacy of this block in spinal surgeries is equivocal. Recently published reviews on this issue have concerning limitations in methodology.MethodsA systematic search was conducted using the PubMed, Scopus, Embase, and Cochrane Central Register of Controlled Trials (CENTRAL). Randomized controlled trials (RCTs) that were done in patients undergoing spinal surgery and had compared outcomes of interest among those that received ESPB and those with no block/placebo were considered for inclusion. Statistical analysis was performed using STATA software. GRADE assessment was done for the quality of pooled evidence.ResultsA total of 13 studies were included. Patients receiving ESPB had significantly reduced total opioid use (Standardized mean difference, SMD −2.76, 95% CI: −3.69, −1.82), need for rescue analgesia (Relative risk, RR 0.38, 95% CI: 0.22, 0.66) and amount of rescue analgesia (SMD −5.08, 95% CI: −7.95, −2.21). Patients receiving ESPB reported comparatively lesser pain score at 1 h (WMD −1.62, 95% CI: −2.55, −0.69), 6 h (WMD −1.10, 95% CI: −1.45, −0.75), 12 h (WMD −0.78, 95% CI: −1.23, −0.32) and 24 h (WMD −0.54, 95% CI: −0.83, −0.25) post-operatively. The risk of postoperative nausea and vomiting (PONV) (RR 0.32, 95% CI: 0.19, 0.54) was lower in those receiving ESPB. There were no differences in the duration of surgery, intra-operative blood loss and length of hospital stay between the two groups. The quality of pooled findings was judged to be low to moderate.ConclusionsESPB may be effective in patients with spinal surgery in reducing post-operative pain as well as need for rescue analgesic and total opioid use. In view of the low to moderate quality of evidence, more trials are needed to confirm these findings.Systematic Review Registration:http://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42021278133.
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