矮化中间砧‘宫藤富士’苹果栽植密度对树体生长、冠层光照和果实产量的影响

2011 年春季定植的矮化中间砧苹果成品苗（3 年根 1 年干的‘宫藤富士’/SH6/平邑甜茶）为试材，设置 7 种不同的栽植密度（株行距分别为 1 m × 3 m、1.5 m × 3 m、2 m × 3 m、0.75 m × 4 m、1 m × 4 m、1.25 m × 4 m 和 1.5 m × 4 m），细纺锤形整枝修剪，自栽植第 2 年，连续 7 年调查 7 种栽植密度对树体生长、冠层光照分布、果实产量和品质的影响。随着树龄的增长，不同栽植密度下树干粗度和总枝量逐年增加，不同处理间树干粗度无显著差异，第 7 年 1 m × 3 m 和 0.75 m × 4 m 两个栽植密度下树体总枝量超过 140 万条 · hm-2，第 8 年均超过 140 万条 · hm-2。栽植前期（第 2 ~ 4 年）各栽植密度树体短枝比例不断增加，长枝比例不断减少，第 5 年各栽植密度枝类组成趋于稳定；综合稳产 3 年（第 6 ~ 8 年）树体的枝类组成数据，4 m 行距的短枝比例明显高于 3 m 行距，长枝比例略低。树体冠层平均相对光照强度由高到低的株行距处理依次为 1.5 m × 4 m（63.87%）、1.25 m × 4 m（61.44%）、2 m × 3 m（61.27%）、1 m × 4 m（59.19%）、0.75 m × 4 m（55.79%）、1.5 m × 3 m（53.67%）和 1 m × 3 m（49.37%）；相同栽植株数下，4 m 行距处理低光效（相对光照强度小于 40%）的区域比例显著小于 3 m 行距。比较前 5 年的累计产量，以行距 4 m 和 1 m × 3 m 的最高。综合稳产 3 年的结果情况，大果率（单果质量 > 200 g 的果实产量占总产量的比例）以 4 m 行距和 2 m × 3 m 的最高。各栽植密度下的果实的可溶性固形物含量、固酸比、果形指数和果实硬度均无显著差异。综上，采用 4 m 行距，1 ~ 1.25 m 株距，树体成形快，稳产后树体结构合理，冠层光照充足，低效光区比例少，前期产量高。     

Advances in function of circular RNA and regulation of atherosclerosis development

Atherosclerosis is one of the cardiovascular diseases that seriously endanger human health. The pathogenesis of atherosclerosis is very complicated and related to a variety of risk factors. In recent years, many studies have found that circular RNAs play an important regulatory role in the occurrence and development of atherosclerosis by inducing proliferation, differentiation, migration and apoptosis of vascular smooth muscle cells, endothelial cells and macrophages. This article reviews the basic functions of circular RNAs and its recent research on the regulation of atherosclerosis.     

Progress of STIM1, a dynamic calcium signal transducer, #br# in cardiovascular diseases

Stromal interaction molecule 1 (STIM1) is a transmembrane protein of the endoplasmic reticulum (ER), a Ca²⁺ transducer in ER that activates the store-operated calcium channel. Through Orai1 protein, STIM1 adjusts the intracellular and extracellular calcium concentration. This way is called a store-operated Ca²⁺ entry. STIM1 plays a key role in phenotypic transformation of vascular smooth muscle cells, proliferation of endothelial cells, myocardial hypertrophy and myocardial fibrosis to regulate lots of cardiovascular diseases, such as atherosclerosis, congestive heart failure and systemic hypertension. STIM1 is closely related to cardiovascular diseases through calcium signal. The research progress of STIM1 in cardiovascular diseases is mainly discussed in this article.     

Lysophosphatidic acid and phenotypic modulation in vascular smooth muscle cells

Lysophosphatidic acid (LPA) is a sort of phospholipid messenger possessing diverse physiological role, which is mediated by its G protein-coupled receptors, and plays a significant role in vascular diseases. Phenotypic modulation of vascular smooth muscle cells (VSMCs) is the key initiation step of VSMCs proliferation and migration in hypertension, atherosclerosis and postangioplasty restenosis, and is the common morbility foundation of these vascular diseases. In this article we briefly review the LPA biological characteristics, its relationship with VSMCs phenotypic modulation and relative signal transduction pathway.     

Recent advances in the study of G protein-coupled receptor 40/free fatty acid receptor 1

Free fatty acids (FFAs) provide an important energy source and also act as signaling molecules. Medium to long-chain free fatty acids can activate the intracellular signal pathways in the pancreatic β-cells and play a role in regulating insulin secretion as an extracellular signal molecular via binding to the FFA receptor G protein-coupled receptor 40 (GPR40). Furthermore, GPR40 is associated with several biological effects including cell proliferation and antiapoptosis of nerve cells. GPR40 act an important role in the connection of obesity and diabetes or cancers. GPR40 will probably become a novel kind of antidiabetic and anticancer drugs.     

Role of GPR40 mediates the effects of FFAs on lipoapoptosis in mouse β-cell line NIT-1

AIM: To evaluate the role of G protein-coupled receptor 40 (GPR40) mediates the effects of free fatty acids (FFAs) on lipoapoptosis in mouse β-cell line NIT-1 and the mechanisms involved in this process.METHODS: NIT-1 cells were supplemented with palmitate (500 μmol/L) or oleate (500 μmol/L) for 48 h, then apoptosis of the cells was determined by the methods of Hoechst 33342, TUNEL and flow cytometry (Annexin V/PI). The small interfering RNA technique was used to inhibit the expression of GPR40 in NIT-1 cell. The mock, control siRNA and GPR40 siRNA transfected cells were either supplemented with palmitate (500 μmol/L) or co-incubated with palmitate and oleate (500 μmol/L for each) for 48 h. The percentages of apoptotic cells were quantified. The expression of p-c-Jun, Bcl-2 and Bax were detected by Western blotting.RESULTS: Palmitate induced β cell lipoapoptosis, whereas oleate inhibited NIT-1 cells from palmitate-induced lipoapoptosis. No significant difference of the percentages of apoptotic cells was indicated among the mock, control siRNA and GPR40 siRNA transfected cells treated with palmitate (P>0.05). However, after co-incubated with palmitate and oleate (500 μmol/L for each) for 48 h, the percentage of apoptotic cells in GPR40 siRNA transfected cells was greater than that in mock (P<0.05), while the expression of p-c-Jun was decreased. The expressions of Bcl-2 and Bax were not affected.CONCLUSION: Palmitate induced β cell lipoapoptosis might not be mediated through GPR40, whereas oleate inhibits NIT-1 cells from palmitate-induced lipoapoptosis, which is mediated at least in part through GPR40, the change of c-Jun expression may play an role in this process, suggesting that GPR40 might be implicated in the control of β cell mass plasticity and GPR40 probably provides a link between obesity and type 2 diabetes.     

Progress in role of lncRNA in cardiovascular diseases

Cardiovascular diseases are closely related to proliferation, injury and apoptosis of the cells in the cardiovascular system. For instance, endothelial cells play an important role in the pathogenic process of hypertension and atherosclerosis, and smooth muscle cells and monocytes/macrophages involve in the formation of atherosclerotic plaque. Recently, it has been confirmed that long noncoding RNA (lncRNA) regulates proliferation, apoptosis, injury, autophagy and differentiation of the cells by a series of regulatory mechanisms, thus participating in the development and progression of cardiovascular diseases. This article is to review the recent research progress on the function of lncRNAs and their regulatory roles in the cardiovascular diseases at cellular and molecular levels.     

Research progress in association between angiopoietin-like protein 2 and inflammation-related diseases

Chronic low-grade inflammatory diseases are a subclinical process caused by innate system disorders. In recent years, with the study of chronic low-grade inflammatory diseases, inflammation has become a hot topic of major human diseases, including obesity, diabetes, cardiovascular diseases, cancer and autoimmune diseases. Angiopoietin-like protein 2 (ANGPTL2) is one of the emerging angiogenesis-related factors. Studies show that ANGPTL2 induces vascular inflammation, insulin resistance and other characteristics. The article reviews the research progress in association between angiopoietin-like protein 2 and inflammation-related diseases.     

Recent advances in artrial elastin

The elastin has been investigated since the 1950s, and it has been found that elastin relates to the vascular diseases in recent years. In this review, the elastin gene structure, distribution and its role in the pathogenesis of vascular diseases and aging are summarized.     

Effects of anti-cardiac AT1-receptor antibody on ventricular myocyte ionic currents in rats

AIM: In an attempt to clarify the role of anti-angiotensinⅡ-receptor antibody (anti AT₁-R Ab) in the pathogenesis of cardiovascular diseases, the effects of AT₁-R Ab on several major ionic currents in rat ventricular myocytes were studied.METHODS: The anti-AT₁-R Ab was derived by immunizing rats with synthetic peptide corresponding to the sequence of the second extracellular loop of human AT₁ receptor. Whole cell patch clamp was used to measure the ionic currents including I_Ca-L, I_Na/Ca, I_to, and I_K1 in the rat ventricular myocytes.RESULTS: AT₁-R Ab IgG significantly increased the I_Ca-L and I_Na/Ca, but decreased the I_to and I_k1 in a dose-dependent manner. Compared with the control, all these differences were statistically significant. These effects of anti-AT₁-R Ab were in the same way as the effects of AngⅡ, an agonist of AT₁-R, and were blocked by losartan, a specific antagonist of AT₁-R.CONCLUSION: Anti-AT₁-R Ab displays remarkable agonist-like activity on the ionic currents in cardiomyocytes via stimulation of AT₁-R and increase of calcium influx, and therefore affects the cardiac activity. These findings indicate that AT₁-R Ab is involved in the pathogenesis of cardiovascular diseases.     

Mechanism of renin release and renin inhibitors

The renal local renin-angiotensin system (RAS) plays a key role in regulating the balance of water, electrolytes and blood pressure. Release of renin is the rate-limiting step of RAS activation. Recent studies have found that G-protein-coupled receptor 91 (GPR91) is highly expressed in the kidney, and can be activated by succinate, causing renin release. In recent years, from the source of renin to block the activation of RAS has become a clinical approach. In this paper, the mechanism of succinate/GPR91 to regulate renin release and application of renin inhibitors are reviewed.     

Effects of the antibodies against α1- adrenergic receptor on the proliferation of vascular smooth muscle cells in rats

AIM: The autoantibodies against α1-adrenergic receptor that was found in patients with malignant hypertension, primary hypertension and refractory hypertension has the agonist activity liked the NE, and may play a role in hypertension. In this paper, the effects of this antibody on vascular smooth muscle cell (VSMC) proliferation and its mechanism were to be studied. METHODS: The cultured rat VSMC proliferation induced by the antibodies against α1- adrenergic receptor that was purified by the immune affinity chromatography, was measured by the BrdU cell proliferation assay and cell cycle distribution. The expression of c-jun and c-fos were determined by RT-PCR and Western blotting. RESULTS: Compared to the normal IgG, the antibodies against α1-adrenergic receptor promoted the VSMC proliferation and increased the mRNA and protein expression of the c-jun significantly. The role was similar to the norepinephrine, and all was blocked by prazosin, while the mRNA and protein expression of c-fos were not affected by the antibodies. CONCLUSION: The antibodies against α1-adrenergic receptor promote the rat VSMC proliferation, and increase the expression of c-jun, which maybe play a role in the vascular remodeling in hypertension.     

Progress in function of HDL-eNOS signaling pathway in cardiovascular system and it's influencing factors

High-density lipoprotein (HDL) is negatively related to the risk of cardiovascular diseases such as atherosclerosis. Recent studies have shown that HDL activates a variety of target cells, such as vascular endothelial cells and macrophages, and activates the related cell signaling pathway to exert an anti-atherosclerosis role. HDL is a complex substance which composes of multiple particles. The changes of many factors affect the characteristics and functions of HDL, and then affect the activation of endothelial nitric oxide synthase (eNOS).This paper summarizes the recent correlation studies, and expounds the related factors that affect the HDL-eNOS signaling pathway.     

The stimulating effects of neuropeptide Y on cultured arterial smooth muscle cell proliferation and losartan treatment

AIM:To investigate the interplay between the neuropeptide Y(NPY) and renin-angiotensin system, and relationship to the pathogenesis of hypertension. METHODS: The method of cellular culture, MTT colorimetric assay and quantitative immunocytochemistry through ACAS570 were performed for the effect of neuropeptide Y on proliferation of cultured rat vascular smooth muscle cell (VSMC) and losartan treatment. RESULTS:It was observed that exposure of VSMC to neuropeptide Y could stimulate the proliferation of VSMC and caused increase respectively in MTT OD values and expression of proliferating cell nulear antigen(PCNA) but losartan interfered with NPY stimulating effects on VSMC and decreased MTT OD values and expression of PCNA.CONCLUSION:These results demonstrated that the NPY could promote proliferation of VSMC, this effect was partly preformed through angiotensin Ⅱ receptor.     

Exercise training attenuates hypertension progression via activation of central ACE2-Ang(1-7)-Mas axis in prehypertensive rats

AIM: To investigate the effects of exercise training on the progression from prehypertension to hypertension, blood pressure regulation and the angiotensin-converting enzyme 2 (ACE2)-angiotensin (Ang) (1-7)-MAS axis activation in cardiovascular centers, and to elucidate the central mechanisms of exercise training postponing hypertension progression. METHODS: The male spontaneously hypertensive rats (SHR; n=20, 5 weeks old) and normotensive Wistar Kyoto (WKY) rats (n=20) were randomly assigned to sedentary (Sed) group and exercise training (ExT) group. The trained rats run on a treadmill in moderate-intensity for 20 weeks. Systolic blood pressure (SBP) was measured by tail-cuff method. The baroreflex sensitivity (BRS) was assessed by intravenous injection of phenylephrine. The expression of ACE2 and MAS receptor at mRNA and protein levels in baroreflex centers were determined by real-time PCR and Western blot, respectively. Alterations of BRS were evaluated before and after intracerebroventricular injection of MAS receptor agonist Ang (1-7) and its antagonist A779, respectively. RESULTS: Compared with SHR+Sed group, exercise training since prehypertension significantly postponed the development of hypertension, delayed the hypertension progression, and decreased SBP in both SHR and WKY rats (P<0.05). Exercise training enhanced blood pressure regulation and improved the BRS in SHR (P<0.01). The expression of ACE2 and MAS receptor at mRNA and protein levels in the baroreflex centers (rostral ventrolateral medulla, nucleus tract solitarius and paraventricular nucleus) were up-regulated in SHR+ExT group (P<0.05). Central administration of A779 abolished the benefits of exercise-induced improvement of BRS in SHR+ExT group (P<0.01). In contrast, Ang(1-7) improved the BRS in both SHR+Sed group and SHR+ExT group (P<0.05). CONCLUSION: Exercise training postpones hypertension progression and improves blood pressure regulation, which may be associated with the activation of central ACE2-Ang(1-7)-Mas axis.     

The stimulating effects of neuropeptide Y on cultured arterial smooth muscle cell proliferation and losartan treatment

AIM: To observe expression of proliferating cell nuclear antigen (PCNA), platelet derived growth factor (PDGF) and c-myc in cultured vascular smooth muscle cells which is effected by neuropeptide Y (NPY) and losartan (the receptor blocking agent of angiotensin Ⅱ) therefore exploring effects of NPY on the generation of hypertension and its relationship with losartan reverse treatment in molecular biology. METHODS: Applied the method of quantitative immunocytochemistry through ACAS570. RESULTS: 24 hours exposure of vascular smooth muscle cell to NPY caused an increase in expression of PCNA, PDGF and c-myc respectively. But losartan could reverse these expressions by NPY, decreased the expression of PCNA, PDGF and c-myc.CONCLUSION: NPY is closely related to the generation hypertension. But losartan could reverse these effects of NPR.     

Potassium channels in vascular smooth muscle and essential hypertension

Essential hypertension (EH) is characterized by an increased total peripheral resistance. There are four types of potassium channels in vascular smooth muscle cells, including Kca, Kv, Kir, KATP, which play an important role in regulating the diameter of vascular. The change of potassium channels may have something to do with the pathogenesis of hypertension. This article reviews the characters of potassium channels and their roles in EH.     

Mechanism of endothelial microparticle generation in hypertension and its pathophysiological roles

Hypertension is closely related to many target organ damage. Endothelial microparticles (EMPs), derived from endothelial cells in response to endothelial cell activation or apoptosis, are complex vesicular structures with a membrane skeleton and express various antigens specific to parental endothelial cells. EMPs circulate in human plasma and show elevated levels in many vascular damage diseases, such as hypertension, atherosclerotic vascular diseases, sepsis and diabetes. Recent studies have shown that EMPs could be a comprehensive index for endothelial homeostasis monitoring, such as vasomotor activity, anti-inflammatory status and so on. Especially, more and more evidence suggests that EMPs play an important role in hypertension. Patients with hypertension show higher circulating levels of EMPs compared with healthy controls. Furthermore, increasing evidence demonstrates that EMPs can induce endothelial dysfunction in vitro and in vivo, and then further promote the development of hypertension and its complications. This review will summarize the progress in the definition and formation mechanisms of EMPs, levels of EMPs and their phenotypes in patients with hypertension, and the pathophysiological roles of EMPs in hypertension.     

Role of pentraxin 3 in inflammation and autoimmunity

As a soluble pattern-recognition receptor, pentraxin 3 (PTX3) evolves in various physiological and pathological effects on inflammation, autoimmunity, apoptosis, vessel remodeling, female fertility and vascular endothelial injury. PTX3 is also a sensitive biological marker for detecting severity and activity of various autoimmune diseases. In most cases, PTX3 limits the progress of autoimmunity and plays a protective role in the process of autoimmune diseases.