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Articles by X Ma
Total Records ( 8 ) for X Ma
  H Zhao , Y Wang , Y Wu , X Li , G Yang , X Ma , R Zhao and H. Liu

Hyperlipidemia is regarded as an independent risk factor in the development of ischemic heart disease, and it can increase the myocardial susceptibility to ischemia/reperfusion (I/R) injury. Ischemic postconditioning (Postcon) has been demonstrated to attenuate the myocardial injury induced by I/R in normal conditions. But the effect of ischemic Postcon on hyperlipidemic animals is unknown. Hypoxia inducible factor-1 (HIF-1) has been demonstrated to play a central role in the cardioprotection by preconditioning, which is one of the protective strategies except for Postcon. The aim of this study was to determine whether Postcon could reduce myocardial injury in hyperlipidemic animals and to assess whether HIF-1 was involved in Postcon mechanisms. Male Wistar rats underwent the left anterior descending coronary occlusion for 30 min followed by 180 min of reperfusion with or without Postcon after fed with high fat diet or normal diet for 8 weeks. The detrimental indices induced by the I/R insult included infarct size, plasma creatine kinase activity and caspase-3 activity. Results showed that hyperlipidemia remarkably enhanced the myocardial injury induced by I/R, while Postcon significantly decreased the myocardial injury in both normolipidemic and hyperlipidemic rats. Moreover, both hyperlipidemia and I/R promoted the HIF-1 expression. Most importantly, we have for the first time demonstrated that Postcon further induced a significant increase in HIF-1 protein level not only in normolipidemic but also in hyperlipidemic conditions. Thus, Postcon reduces the myocardial injury induced by I/R in normal and hyperlipidemic animals, and HIF-1 upregulation may involve in the Postcon-mediated cardioprotective mechanisms.

  B Hibbert , X Ma , A Pourdjabbar , E Holm , K Rayner , Y. X Chen , J Sun , L Filion and E. R. O'Brien

Endothelial progenitor cells (EPCs) are circulating pluripotent vascular cells capable of enhancing re-endothelialization and diminishing neointima formation following arterial injury. Glycogen synthase kinase (GSK)-3β is a protein kinase that has been implicated in the regulation of progenitor cell biology. We hypothesized that EPC abundance and function could be enhanced with the use of an inhibitor of GSK-3β (GSKi), thereby resulting in improved arterial repair.

Methods and results

Human EPCs were expanded ex vivo, treated with a specific GSKi, and then assessed for both yield and functional characteristics by in vitro assays for adherence, apoptosis, and survival. In vivo functionality of treated human EPCs was assessed in immune-tolerant mice subjected to femoral artery wire injury. Re-endothelialization was assessed at 72 h and neointima formation at 7 and 14 days following injury. GSKi treatment resulted in an improvement in the yield of EPCs and a reduction in apoptosis in cells derived from both healthy controls and patients with coronary artery disease. Treatment also increased vascular endothelial growth factor secretion, up-regulated expression of mRNA for the -4 integrin subunit, and improved adhesion, an effect which could be abrogated with an -4 integrin blocking antibody. EPCs without or with ex vivo GSKi treatment enhanced re-endothelialization 72 h following injury as well as reduced neointima formation at 7 days (e.g. endothelial coverage: 7.2 ± 1.7% vs. 70.7 ± 5.8% vs. 87.2 ± 4.1%; intima to media ratios: 1.05 ± 0.19 vs. 0.39 ± 0.08 vs. 0.14 ± 0.02; P < 0.05 for all comparisons), an effect that was persistent at 14 days.


GSKi improves the functional profile of EPCs and is associated with improved re-endothelialization and reduced neointima formation following injury.

  X Ma , K Takeda , A Singh , Z. X Yu , P Zerfas , A Blount , C Liu , J. A Towbin , M. D Schneider , R. S Adelstein and Q. Wei

Rationale: Germline ablation of the cytoskeletal protein nonmuscle myosin II (NMII)-B results in embryonic lethality, with defects in both the brain and heart. Tissue-specific ablation of NMII-B by a Cre recombinase strategy should prevent embryonic lethality and permit study of the function of NMII-B in adult hearts.

Objective: We sought to understand the function of NMII-B in adult mouse hearts and to see whether the brain defects found in germline-ablated mice influence cardiac development.

Methods and Results: We used a loxP/Cre recombinase strategy to specifically ablate NMII-B in the brains or hearts of mice. Mice ablated for NMII-B in neural tissues die between postnatal day 12 and 22 without showing cardiac defects. Mice deficient in NMII-B only in cardiac myocytes (BMHC/BMHC mice) do not show brain defects. However, BMHC/BMHC mice display novel cardiac defects not seen in NMII-B germline-ablated mice. Most of the BMHC/BMHC mice are born with enlarged cardiac myocytes, some of which are multinucleated, reflecting a defect in cytokinesis. Between 6 to 10 months, they develop a cardiomyopathy that includes interstitial fibrosis and infiltration of the myocardium and pericardium with inflammatory cells. Four of 5 BMHC/BMHC hearts develop marked widening of intercalated discs.

Conclusions: By avoiding the embryonic lethality found in germline-ablated mice, we were able to study the function of NMII-B in adult mice and show that absence of NMII-B in cardiac myocytes results in cardiomyopathy in the adult heart. We also define a role for NMII-B in maintaining the integrity of intercalated discs.

  S Beddhu , X Ma , B Baird , A. K Cheung and T. Greene

Background and objectives: Serum alkaline phosphatase has been associated with increased mortality in hemodialysis patients but its associations with mortality in chronic kidney disease (CKD) stages III and IV are unknown.

Design, settings, participants & measurements: In 1094 participants in the African-American Study of Kidney Disease and Hypertension (AASK) database, the associations of serum alkaline phosphatase with mortality and cardiovascular events were examined in Cox models.

Results: The mean (±SD) age was 54 ± 11 yr, and 61% were men. The median alkaline phosphatase was 80 IU/L, and interquartile range was 66 to 97 IU/L. The mean follow-up was 4.6 yr. There were 105 (9.6%) all-cause deaths and 149 (13.6%) cardiovascular events. Each doubling of serum alkaline phosphatase was significantly associated with increased hazard [hazard ratio (HR) 1.60, 95% confidence interval (CI) 1.08 –2.36] of all-cause mortality adjusted for demographics, drug and blood pressure groups, and comorbidity. With further adjustment for liver function tests as well as serum calcium and phosphorus, each doubling of serum alkaline phosphatase remained significantly associated with increased mortality (HR 1.55, 95% CI 1.03 to 2.33). Serum alkaline phosphatase was not significantly associated with increased risk of cardiovascular events.

Conclusions: Independent of liver function tests and serum calcium and phosphorus, higher levels of serum alkaline phosphatase are associated with increased mortality in the CKD population. Further studies are warranted to identify the potential mechanisms for this association.

  D Xie , H Bai , L Liu , X Xie , J Ayello , X Ma and J. Zhang

Influenza affects most of the world's population annually, often causing a secondary infection, but pathological mechanisms of influenza virus infection remain unclear. We have found that influenza viruses have a selective preference for infecting monocytes and mature immune effector cells. This paper provides evidence that influenza virus infection increases the expression of granzyme B (GrB) in monocytes, activated T and B cells. All GrB+ cells had cytolytic function. GrB+CD62Lhigh central memory (TCM) cells were fast response population to virus infection when compared with GrB+CD62Llow population. The influenza virus-infected PBMC could be killed by GrB+ cells. We propose the following mechanism for influenza: (i) influenza virus within the respiratory tract overcomes humoral defenses; (ii) free virus is directly engulfed by the immune system effector cells and free virus also infects epithelial cells; (iii) virus-infected epithelial cells and the immune system cells are killed by cytotoxic cells. These indicated that an immune system that was combating a virus infection needs to sacrifice some of its immune system cells. Therefore, influenza viruses might temporally destroy the human immune system's line of defense, resulting in susceptibility to a secondary infection. This might be a prevalent mechanism existing in cell-mediated immune responses.

  X Liu , B Wang , X Ma and Y. Guo

Nuclear factor-B (NF-B) activation has been identified in a variety of solid tumors and lymphoid malignancies. The aim of our study was to determine the expression status and clinical significance of NF-B in extranodal natural killer (NK)/T-cell lymphoma, nasal type.


Tumor specimens from 23 patients with previously untreated NK/T-cell lymphoma initially treated with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) or CHOP-based chemotherapy were examined by immunohistochemistry for three NF-B subunits (p65, p50 and p52), which are involved in either the canonical or alternative pathway.


None of the cases could be detected with p65 or p50 nuclear staining. On the other hand, 15 (65.2%) cases had p52 nuclear staining, suggesting NF-B activation through the alternative pathway. All major clinical characteristics were balanced between NF-B p52-positive and -negative patients. The objective response rate achieved in NF-B-positive patients was significantly lower than that in negative patients (33.3% vs. 87.5%, P = 0.027). At a median follow-up of 25 months, 8 (53.3%) of 15 NF-B-positive patients had died compared with none of 8 NF-B-negative patients (P = 0.041). In a multivariate analysis, NF-B status and stage were identified to be independent prognostic factors.


Our results suggest that NF-B activation through the alternative pathway is frequently observed in NK/T-cell lymphoma and associated with chemoresistance and poor survival.

  B Wang , L Li , F Ni , J Song , J Wang , Y Mu , X Ma and Y. Cao

Pluripotency associated transcription factor, SAL-Like 4 (SALL4), might play an important role in conferring totipotency on oocytes. In the present study, we screened SALL4 coding regions for mutations in 100 Han Chinese women with non-syndromic ovarian failure and discovered two novel non-synonymous variants in the SALL4 gene: c.541G>A (p.Val181Met) and c.2449A>G. (p.Thr817Ala). The former variant was located in an evolutionary conserved region of SALL4 protein and might affect its function. This is the first report to suggest that SALL4 might be a potential candidate gene of premature ovarian failure.

  B Peng , L Cao , X Ma , W Wang , D Wang and L. Yu

Matrix metalloproteinase (MMP) 2, MMP7 and MMP9 are important members of the MMP family. Four polymorphisms in the promoter region of these MMPs, which are MMP2 –1306 C>T, MMP2 –735 C>T, MMP7 –181 A>G and MMP9 –1562 C>T, have been reported to be functional and may contribute to genetic susceptibility to cancers. However, the associations between these polymorphisms and cancer risk remain inconclusive due to conflicting results from different case–control studies. To better evaluate the role of these polymorphisms in cancer development, we conducted a meta-analysis that included 51 studies, with more than 40 000 subjects. The results showed that under dominant genetic model, MMP2 –1306 T was associated with lower susceptibility to lung cancer [odds ratio (OR) = 0.50, 95% confidence interval (CI) 0.43–0.59, Pheterogeneity = 0.147, I2 = 44.1%], head and neck cancer (OR = 0.53, 95% CI 0.41–0.69, Pheterogeneity = 0.974, I2 = 0.0%) and oesophageal cancer (OR = 0.67, 95% CI 0.55–0.80, Pheterogeneity = 0.593, I2 = 0.0%); MMP2-735T was associated with lower risk in lung cancer (OR = 0.65, 95%CI 0.53–0.79, Pheterogeneity = 0.42, I2 = 0.0%) and oesophageal cancer (OR = 0.84, 95% CI 0.70–0.99, Pheterogeneity = 0.206, I2 = 37.4%); MMP7 –181 AG and GG genotype carriers had an increased gastric cancer risk (OR = 1.90, 95% CI 1.43–2.51, Pheterogeneity = 0.992, I2 = 0.0%) and MMP9 –1562 C>T was not associated with cancer risk in the whole group analysis (OR = 0.99, 95% CI 0.91–1.08, Pheterogeneity = 0.419, I2 = 3.0%) and subgroup analyses. In all, our meta-analysis suggests that MMP2 –1306 C>T, MMP2 –735 C>T and MMP7 –181 A>G may play allele-specific roles in cancer development, while MMP9 –1562 C>T may not be a major risk factor for most cancer types. Large case–control studies should be performed to clarify the possible roles of these four polymorphisms in different kinds of cancer in more detail.

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