The role of LR-TIMAP/PP1c complex in the occurrence and development of no-reflow

Quan, Xiaoyu; Liu, Xiucheng; Qin, Xichun; Wang, Yuzhuo; Sun, Tao; Li, Zhimin; Zhu, Liangliang; Chen, Jiali; Zhou, Yeqing; Singh, Sandeep K.; Dong, Hongyan; Zhang, Zhongming; Zhang, Hao

doi:10.1016/j.ebiom.2021.103251

Cited by 12 publications

(7 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…And its expression is restricted to cells involved in circulation, platelets, monocytes, neutrophils, lymphocyte subsets, especially endothelial cells 42 , 43 . In contrast, mM-CD31 is an antibody approximately 130 kDa, which is expressed on platelets and leukocytes, and primarily concentrates at the borders between endothelial cells 44 , 45 . However, the underlying mechanism of the difference between both antibodies still remains elusive.…”

Section: Discussionmentioning

confidence: 99%

The immunolocalization of cluster of differentiation 31, phalloidin and alpha smooth muscle actin on vascular network of normal and ischemic rat brain

Wang

Guo

et al. 2022

Sci Rep

View full text Add to dashboard Cite

Cluster of differentiation 31 (CD31), phalloidin and alpha smooth muscle actin (α-SMA) have been widely applied to label the cerebral blood vessels in the past years. Although CD31 is mainly used as endothelial marker in determining the cerebral capillaries, it seems likely that its labeling efficiency is closely correlated with the antibodies from the polyclonal or monoclonal one, as well as the conditions of blood vessels. In order to test this phenomenon, we compared the labeling characteristics of goat polyclonal anti-CD31 (gP-CD31) and mouse monoclonal anti-CD31 (mM-CD31) with those of phalloidin and α-SMA on the rat brain in health and ischemia/reperfusion (I/R) with the middle cerebral artery occlusion. By multiple immunofluorescence staining, it was found that gP-CD31 labeling expressed extensively on the cerebral capillaries forming the vascular networks on the normal and ischemic regions, but mM-CD31 labeling mainly presented on the capillaries in the ischemic region. In contrast to the vascular labeling with gP-CD31, phalloidin and α-SMA were mainly expressed on the wall of cortical penetrating arteries, and less on that of capillaries. By three-dimensional reconstruction analysis, it was clearly shown that gP-CD31 labeling was mainly located on the lumen side of vascular wall and was surrounded by phalloidin labeling and α-SMA labeling. These results indicate that gP-CD31 is more sensitive than mM-CD31 for labeling the cerebral vasculature, and is highly compatible with phalloidin and α-SMA for evaluating the cerebral vascular networks under the physiological and pathological conditions.

show abstract

Section: Discussionmentioning

confidence: 99%

The immunolocalization of cluster of differentiation 31, phalloidin and alpha smooth muscle actin on vascular network of normal and ischemic rat brain

Wang

Guo

et al. 2022

Sci Rep

View full text Add to dashboard Cite

show abstract

“…NR's pathogenetic components are extremely complicated. Local swelling of endothelium and cardiomyocytes, breaches in the endothelial continuity, microvascular bleeding, thrombosis, interstitial edema, and inflammation in the NR zones have all been observed in experimental experiments (Quan et al, 2021).…”

Section: Discussionmentioning

confidence: 85%

“…The presence of NR can expand the risk of major adverse cardiovascular occasions and is widely considered a major marker of poor prognosis. Researchers all across the world are working to improve the prevention, management, and therapy of the NR phenomenon after percutaneous coronary intervention (PCI) (Quan et al, 2021) (Quan et al, 2021). The endothelium's barrier function, on the other hand, is necessary for adequate blood-tissue exchange and homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Shenlian extract decreases mitochondrial autophagy to regulate mitochondrial function in microvascular to alleviate coronary artery no‐reflow

Wang

et al. 2023

Phytotherapy Research

View full text Add to dashboard Cite

Shenlian (SL) extract has been proven to be effective in the prevention and treatment of atherosclerosis and myocardial ischemia. However, the function and molecular mechanisms of SL on coronary artery no‐reflow have not been fully elucidated. This study was designed to investigate the contribution of SL extract in repressing excessive mitochondrial autophagy to protect the mitochondrial function and prevent coronary artery no‐reflow. The improvement of SL on coronary artery no‐reflow was observed in vivo experiments and the molecular mechanisms were further explored through vitro experiments. First, a coronary artery no‐reflow rat model was built by ligating the left anterior descending coronary artery for 2 hr of ischemia, followed by 24 hr of reperfusion. Thioflavin S (6%, 1 ml/kg) was injected into the inferior vena cava to mark the no‐reflow area. Transmission electron microscopy was performed to observe the cellular structure, mitochondrial structure, and mitochondrial autophagy of the endothelial cells. Immunofluorescence was used to observe the microvascular barrier function and microvascular inflammation. Cardiac microvascular endothelial cells (CMECs) were isolated from rats. The CMECs were deprived of oxygen–glucose deprivation (OGD) for 2 hr and reoxygenated for 4 hr to mimic the Myocardial ischemia‐reperfusion (MI/R) injury‐induced coronary artery no‐reflow in vitro. Mitochondrial membrane potential was assessed using JC‐1 dye. Intracellular adenosine triphosphate (ATP) levels were determined using an ATP assay kit. The cell total reactive oxygen species (ROS) levels and cell apoptosis rate were analyzed by flow cytometry. Colocalization of mitochondria and lysosomes indirectly indicated mitophagy. The representative ultrastructural morphologies of the autophagosomes and autolysosomes were also observed under transmission electron microscopy. The mitochondrial autophagy‐related proteins (LC3II/I, P62, PINK, and Parkin) were analyzed using Western blot analysis. In vivo, results showed that, compared with the model group, SL could reduce the no‐reflow area from 37.04 ± 9.67% to 18.31 ± 4.01% (1.08 g·kg−1 SL), 13.79 ± 4.77% (2.16 g·kg−1 SL), and 12.67 ± 2.47% (4.32 g·kg−1 SL). The extract also significantly increased the left ventricular ejection fraction (EF) and left ventricular fractional shortening (FS) (p < 0.05 or p < 0.01). The fluorescence intensities of VE‐cadherin, which is a junctional protein that preserves the microvascular barrier function, decreased to ~74.05% of the baseline levels in the no‐reflow rats and increased to 89.87%(1.08 g·kg−1SL), 82.23% (2.16 g·kg−1 SL), and 89.69% (4.32 g·kg−1 SL) of the baseline levels by SL treatment. SL administration repressed the neutrophil migration into the myocardium. The oxygen–glucose deprivation/reoxygenation (OGD/R) model was induced in vitro to mimic microvascular ischemia–reperfusion injury. The impaired mitochondrial function after OGD/R injury led to decreased ATP production, calcium overload, the excessive opening of the Mitochond...

show abstract

“…HCMECs play crucial physiological roles in maintaining the normal function of the heart, and their dysfunction leads to various cardiovascular diseases, such as ischemic cardiomyopathy, diabetic cardiomyopathy, myocardial infarction and heart failure ( 30 – 32 ). Human umbilical vein endothelial cells and human coronary artery endothelial cells have been used to investigate EndMT ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00961 regulates endothelial‑mesenchymal transition via the PTEN‑PI3K‑AKT pathway

Zheng

Ting

et al. 2022

Mol Med Rep

View full text Add to dashboard Cite

The long noncoding RNA LINC00961 plays a crucial role in cancer and cardiovascular diseases. In the present study, the role and underlying mechanism of LINC00961 in endothelial-mesenchymal transition (EndMT) induced by transforming growth factor beta (TGF-β), was investigated. Human cardiac microvascular endothelial cells were transfected with LV-LINC00961 or short hairpin LINC00961 plasmids to overexpress or knock down LINC00961 in the cells, respectively. The cells were then exposed to TGF-β in serum-free medium for 48 h to induce EndMT. Flow cytometric analysis, Cell Counting Kit-8 assay and immunofluorescence staining were performed to examine the cell apoptosis rate, assess cell viability, and identify CD31 + /α-SMA + double-positive cells, respectively. Western blotting and reverse transcription- quantitative polymerase chain reaction were used to evaluate protein and mRNA expression, respectively. Injury to endothelial cells and EndMT was induced by TGF-β in a time-dependent manner. LINC00961 overexpression promoted injury and EndMT, whereas LINC00961 knockdown had the opposite effects. Knockdown of LINC00961 attenuated EndMT and injury to endothelial cells induced by TGF-β via the PTEN-PI3K-AKT pathway. Inhibition of LINC00961 expression may prevent the occurrence of EndMT-related cardiovascular diseases, such as myocardial fibrosis and heart failure. Therefore, LINC00961 shows potential as a therapeutic target for cardiovascular diseases.

show abstract

The role of LR-TIMAP/PP1c complex in the occurrence and development of no-reflow

Cited by 12 publications

References 39 publications

The immunolocalization of cluster of differentiation 31, phalloidin and alpha smooth muscle actin on vascular network of normal and ischemic rat brain

The immunolocalization of cluster of differentiation 31, phalloidin and alpha smooth muscle actin on vascular network of normal and ischemic rat brain

Shenlian extract decreases mitochondrial autophagy to regulate mitochondrial function in microvascular to alleviate coronary artery no‐reflow

LncRNA LINC00961 regulates endothelial‑mesenchymal transition via the PTEN‑PI3K‑AKT pathway

Contact Info

Product

Resources

About