Coronary angiography review in 21 children with Kawasaki disease complicated with coronary artery disease

Objective·To analyze the progression of children with severe coronary artery lesions due to Kawasaki disease by coronary artery angiography, and evaluate the diagnostic value of echocardiography in these children.Methods·A retrospective analysis was performed to enroll children with Kawasaki disease whose coronary artery lesions were graded Ⅳ or above from Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, from January 2013 to January 2023. The subjects were required to have received at least 2 times of coronary angiogram, and their clinical and imaging data were collected to analyze the progression of the lesions. Echocardiography results were compared with the results of the coronary angiogram.Results·A total of 21 children were included, including 15 males and 6 females, with a median age at onset of 3 years and 6 months, a median age at initial coronary angiography of 7 years and 11 months, a median interval of 4 years and 5 months between the time of onset and initial angiography, a median age at angiographic review of 9 years and 2 months, and a median interval of 1 year and 3 months between the time of initial angiography and review. Coronary stenosis or occlusion was detected in 13 children in the initial angiography, of whom 6 underwent coronary artery bypass grafting (CABG) and had their angiography reviews 1 year later. The review results showed that the bridging vessels were unobstructed and no obvious stenosis was observed. Fifteen children had progression of the lesions detected by echocardiography in the subsequent follow-up and had their angiogram reviews, of whom 8 had significant progression of the coronary lesions. Intracoronary balloon dilatation was performed in 1 case, and CABG was performed in another case. Sixteen lesions of coronary stenosis or occlusion were detected in the initial angiography in 21 children, while only 1 lesion of coronary stenosis was detected by echocardiography during the same period of time. Twenty-eight medium- to large-sized coronary aneurysms were detected in the initial angiography in the 21 children, and the diameters of the 28 aneurysms measured by echocardiography and coronary angiogram were subjected to the Bland-Altman analysis. The Bland-Altman analysis showed that the difference in maximum diameter between 2 methods was (1.63±2.33) mm, with 95%CI of -2.95‒6.21 mm.Conclusion·Coronary artery lesions due to Kawasaki disease may be progressive; in the children with severe lesions, coronary artery stenosis or occlusion may be missed or misdiagnosed and some errors may exist in the measurement of diameters of aneurysms by echocardiography. Regular review of coronary angiography is needed

Vegfa Impacts Early Myocardium Development in Zebrafish

Vascular endothelial growth factor A (Vegfa) signaling regulates cardiovascular development. However, the cellular mechanisms of Vegfa signaling in early cardiogenesis remain poorly understood. The present study aimed to understand the differential functions and mechanisms of Vegfa signaling in cardiac development. A loss-of-function approach was utilized to study the effect of Vegfa signaling in cardiogenesis. Both morphants and mutants for vegfaa display defects in cardiac looping and chamber formation, especially the ventricle. Vegfa regulates the heart morphogenesis in a dose-dependent manner. Furthermore, the initial fusion of the bilateral myocardium population is delayed rather than endocardium. The results demonstrate that Vegfa signaling plays a direct impact on myocardium fusion, indicating that it is the initial cause of the heart defects. The heart morphogenesis is regulated by Vegfa in a dose-dependent manner, and later endocardium defects may be secondary to impaired myocardium–endocardium crosstalk

Vegfa Impacts Early Myocardium Development in Zebrafish

Vascular endothelial growth factor A (Vegfa) signaling regulates cardiovascular development. However, the cellular mechanisms of Vegfa signaling in early cardiogenesis remain poorly understood. The present study aimed to understand the differential functions and mechanisms of Vegfa signaling in cardiac development. A loss-of-function approach was utilized to study the effect of Vegfa signaling in cardiogenesis. Both morphants and mutants for vegfaa display defects in cardiac looping and chamber formation, especially the ventricle. Vegfa regulates the heart morphogenesis in a dose-dependent manner. Furthermore, the initial fusion of the bilateral myocardium population is delayed rather than endocardium. The results demonstrate that Vegfa signaling plays a direct impact on myocardium fusion, indicating that it is the initial cause of the heart defects. The heart morphogenesis is regulated by Vegfa in a dose-dependent manner, and later endocardium defects may be secondary to impaired myocardium–endocardium crosstalk

Regulation of Tight Junctions by Sex Hormones in Goat Mammary Epithelial Cells

The sex hormones of estrogen and progesterone (P4) play a vital role in mammary gland development and milk lactation in ruminants. The tight junction (TJ) between adjacent secretory epithelial cells is instrumental in establishing the mammary blood–milk barrier. However, whether estrogen and P4 exert their effect on mammary function via regulating TJ remain unclear. Here, to clarify the role of 17-β estradiol (E2) and P4 in the regulation of TJ in goat mammary gland, we first explored the relationships between the concentrations of E2, P4, and the protein expression of claudin-1, claudin-3, occludin, and ZO-1 during the mammary gland development in goat. Then, we further explored the mRNA and protein expression of claudin-1, claudin-3, occludin, and ZO-1 in the goat mammary epithelial cells (GMECs) in vitro under different concentrations of E2 and P4. The results demonstrated that the protein expression of claudin-1 decreased, but occludin and ZO-1 increased with the decline in E2 and P4 during the transition from pregnancy to lactation. In the in vitro studies, E2 exerted a positive effect on the mRNA expression of claudin-1, and accelerated the proteins’ expression of claudin-1 and ZO-1 in GMECs; P4 upregulated the mRNA expression of claudin-1, claudin-3, occludin, and ZO-1, and also improved the protein expression of claudin-1, claudin-3, and ZO-1 in the GMECs. The results demonstrated that E2 and P4 play an important role in regulating the expression of the mammary TJ components, which may ultimately affect the mammary gland development and milk lactation

Essential Role of CRIM1 on Endometrial Receptivity in Goat

In domestic ruminants, endometrial receptivity is related to successful pregnancy and economic efficiency. Despite several molecules having been reported in the past regarding endometrial receptivity regulation, much regarding the mechanism of endometrial receptivity regulation remains unknown due to the complex nature of the trait. In this work, we demonstrated that the cysteine-rich transmembrane bone morphogenetic protein (BMP) regulator 1 (CRIM1) served as a novel regulator in the regulation of goat endometrial receptivity in vitro. Our results showed that hormones and IFN-τ increased the expression of CRIM1 in goat endometrial epithelial cells (EECs). Knockdown of CRIM1 via specific shRNA hindered cell proliferation, cell adhesion and prostaglandins (PGs) secretion and thus derailed normal endometrial receptivity. We further confirmed that receptivity defect phenotypes due to CRIM1 interference were restored by ATG7 overexpression in EECs while a loss of ATG7 further impaired receptivity phenotypes. Moreover, our results showed that changing the expression of ATG7 affected the reactive oxygen species (ROS) production. Moreover, mR-143-5p was shown to be a potential upstream factor of CRIM1-regulated endometrial receptivity in EECs. Overall, these results suggest that CRIM1, as the downstream target of miR-143-5p, has effects on ATG7-dependent autophagy, regulating cell proliferation, cell adhesion and PG secretion, and provides a new target for the diagnosis and treatment of early pregnancy failure and for improving the success rates of artificial reproduction