The Different Expression Patterns of HSP22, a Late Embryogenesis Abundant-like Protein, in Hypertrophic H9C2 Cells Induced by NaCl and Angiotensin II

BACKGROUND: High-NaCl diet is a contributing factor for cardiac hypertrophy. The role of HSP22 as a protective protein during cardiac hypertrophy due to hypernatremia is unclear. Accordingly, this study aimed to establish a cellular hypernatremic H9C2 model and to compare the expression of HSP22 in Ca2+ homeostasis between a high-NaCl and angiotensin II-induced hypertrophic cellular H9C2 model. METHODS: Real-time PCR was performed to compare the mRNA expression. Flow cytometry and confocal microscopy were used to analyze the cells. RESULTS: The addition of 30 mM NaCl for 48 h was the most effective condition for the induction of hypertrophic H9C2 cells (termed the in vitro hypernatremic model). Cardiac cellular hypertrophy was induced with 30 mM NaCl and 1 µM angiotensin II for 48 h, without causing abnormal morphological changes or cytotoxicity of the culture conditions. HSP22 contains a similar domain to that found in the consensus sequences of the late embryogenesis abundant protein group 3 from Artemia. The expression of HSP22 gradually decreased in the in vitro hypernatremic model. In contrast to the in vitro hypernatremic model, HSP22 increased after exposure to angiotensin II for 48 h. Intracellular Ca2+ decreased in the angiotensin II model and further decreased in the in vitro hypernatremic model. Impaired intracellular Ca2+ homeostasis was more evident in the in vitro hypernatremic model. CONCLUSION: The results showed that NaCl significantly decreased HSP22. Decreased HSP22, due to the hypernatremic condition, affected the Ca2+ homeostasis in the H9C2 cells. Therefore, hypernatremia induces cellular hypertrophy via impaired Ca2+ homeostasis. The additional mechanisms of HSP22 need to be explored further.

A new compound from roots and rhizomes of Helleborus thibetanus / 中草药

Objective: To study the chemical constituents in the ethanol extract from the roots and rhizomes of Helleborus thibetanus. Methods: The compounds were isolated and purified by silica gel column chromatography and recrystallization. The structures of the compounds were identified on the basis of chemical and spectral methods. Results: A new compound was isolated from the ethanol extract in the roots and rhizomes of H. thibetanus and identified as 14β-hydroxy-3β - [(β-D-glucopyranosyl)oxy]-5α-bufa-20, 22-dienolide (1). Conclusion: Compound 1 is a new compound named as hellebocoside A, which belongs to bufadienolide of cardiac glycosides.

Prenatal Diagnosis of Chromosome 22q11.2 Deletions: Experiences in a Single Institution

PURPOSE: This study was designed to determine the frequency and echocardiographic findings of 22q11.2 deletions in fetuses with cardiac defects on fetal ultrasound or familial backgrounds of 22q11.2 deletions. MATERIALS AND METHODS: We retrospectively reviewed the medical and ultrasonographic records of 170 fetuses that underwent fluorescence in situ hybridization (FISH) analysis for chromosome 22q11.2 deletions between February 2001 and April 2013. RESULTS: Among 145 fetuses with cardiac defects, six (4.1%) had 22q11.2 deletions. Deletions of 22q11.2 were detected in 6 (5%) of the 120 fetuses with conotruncal defects: 5 (8.9%) of 56 with tetralogy of Fallot (TOF) and 1 (5.9%) of 17 with double outlet right ventricle (DORV). No deletions were found in cases of pulmonary atresia, truncus arteriosus, right aortic arch, or transposition of the great arteries. No 22q11.2 deletions were found in non-conotruncal cardiac malformations. Among 25 fetuses with familial backgrounds of 22q11.2 deletions, one (4%) had a maternally inherited 22q11.2 deletion with no cardiac findings. CONCLUSION: Knowledge of the frequency and echocardiographic findings of 22q11.2 deletions might be helpful for prenatal genetic counseling. It is advisable to perform FISH analysis for 22q11.2 deletions in pregnancies exhibiting conotruncal cardiac defects such as TOF or DORV.

Significance of screening chromosome 22q11.2 deletion syndrome in the congenital cardiovascular abnormalities / 国际儿科学杂志

Chromosome 22q11.2 deletion syndrome,also called DiGeorge syndrome or Velo-CardiacFacial syndrome,has all expansive phenotype involving essentially every organ and system,such as cardiovascular abnormalities,abnormal face,immunodeficiency,even psychiatric illnesses,and etc.Fluorescence in situ hybridization analysis test for the microdeletion from chromosome 22 at the q11.2 band is the comqrmed diagnostic method So far,it has not been known thoroughly in China and there has not been a normative screening system yet.Close relations between the microdeletion and congenital cardiovascular abnormalities especially conotruncal cardiac defects and arcus aortae abnormalities have been shown in reported cases.This review will describe the 22q11 DS and how to screen it in the congenital cardiovascular abnormalities so that it Can be diagnosed early and managed properly.which will benefit the patients and their later generations.

Long-term effectiveness of biventricular pacing therapy in patients with congestive heart failure of different etiology / 中国介入心脏病学杂志

60 mm and left ventricular ejection fraction (LVEF)