Dr.  zongxian Jiao

Biography

Dr.  Zongxian Jiao is currently working as a Professor in the Department of Medical sciences, Lanzhou University , china. His research interests includes Chronic obstructive pulmonary disease (COPD) is a worldwide leading cause of morbidity and mortality and its prevalence is still rising. It is therefore important to understand the development of this disease in order to develop strategies of prevention, treatment, and cure. Cigarette smoke extract (CSE) is a complex mixture of chemicals containing high levels of oxidants and is the major etiologic factor in the development of COPD, of which emphysema is a major component. Among the various cell types which compose the lung, the epithelial cells of the alveolar structure appear to be a major target for oxidant injury. It is now well established that type II cells are the stem cells of the alveolar epithelium. After oxidant injury, the rapidity of initiation of type II cell proliferation is crucial for a proper healing. Therefore, characterization of the mechanisms involved in the block of type II cell replication by oxidants and in its reversibility appears to be critical for the understanding and management of many lung diseases associated with oxidative stress. In previous studies, several components of the insulin-like growth factor (IGF) system have been reported involved in the control of proliferation by using a rat type II epithelial cell line, Particularly, accumulation of the IGF binding protein (IGFBP)-2 was associated with block of type II cell proliferation caused by hyperoxia, serum deprivation and glucocorticoid and so on. However the mechanisms regulating human alveolar type II epithelial cell replication upon cigarette smoke exposure remain poorly understood. To provide information on the influence of CSE on the repair capacity of the alveolar epithelium, I am interested in analyzing the effect of CSE on the proliferative response of alveolar type II epithelial cells. To document any protective role of retinoic acid (RA) to reverse the CSE effect, we are to examine the consequence of RA treatment on CSE-induced growth inhibition of type II epithelial cells。. He /she is serving as an editorial member and reviewer of several international reputed journals. Dr.  Zongxian Jiao is the member of many international affiliations. He/ She has successfully completed his Administrative responsibilities. He /she has authored of many research articles/books related to Chronic obstructive pulmonary disease (COPD) is a worldwide leading cause of morbidity and mortality and its prevalence is still rising. It is therefore important to understand the development of this disease in order to develop strategies of prevention, treatment, and cure. Cigarette smoke extract (CSE) is a complex mixture of chemicals containing high levels of oxidants and is the major etiologic factor in the development of COPD, of which emphysema is a major component. Among the various cell types which compose the lung, the epithelial cells of the alveolar structure appear to be a major target for oxidant injury. It is now well established that type II cells are the stem cells of the alveolar epithelium. After oxidant injury, the rapidity of initiation of type II cell proliferation is crucial for a proper healing. Therefore, characterization of the mechanisms involved in the block of type II cell replication by oxidants and in its reversibility appears to be critical for the understanding and management of many lung diseases associated with oxidative stress. In previous studies, several components of the insulin-like growth factor (IGF) system have been reported involved in the control of proliferation by using a rat type II epithelial cell line, Particularly, accumulation of the IGF binding protein (IGFBP)-2 was associated with block of type II cell proliferation caused by hyperoxia, serum deprivation and glucocorticoid and so on. However the mechanisms regulating human alveolar type II epithelial cell replication upon cigarette smoke exposure remain poorly understood. To provide information on the influence of CSE on the repair capacity of the alveolar epithelium, I am interested in analyzing the effect of CSE on the proliferative response of alveolar type II epithelial cells. To document any protective role of retinoic acid (RA) to reverse the CSE effect, we are to examine the consequence of RA treatment on CSE-induced growth inhibition of type II epithelial cells。.

Research Interest

Chronic obstructive pulmonary disease (COPD) is a worldwide leading cause of morbidity and mortality and its prevalence is still rising. It is therefore important to understand the development of this disease in order to develop strategies of prevention, treatment, and cure. Cigarette smoke extract (CSE) is a complex mixture of chemicals containing high levels of oxidants and is the major etiologic factor in the development of COPD, of which emphysema is a major component. Among the various cell types which compose the lung, the epithelial cells of the alveolar structure appear to be a major target for oxidant injury. It is now well established that type II cells are the stem cells of the alveolar epithelium. After oxidant injury, the rapidity of initiation of type II cell proliferation is crucial for a proper healing. Therefore, characterization of the mechanisms involved in the block of type II cell replication by oxidants and in its reversibility appears to be critical for the understanding and management of many lung diseases associated with oxidative stress. In previous studies, several components of the insulin-like growth factor (IGF) system have been reported involved in the control of proliferation by using a rat type II epithelial cell line, Particularly, accumulation of the IGF binding protein (IGFBP)-2 was associated with block of type II cell proliferation caused by hyperoxia, serum deprivation and glucocorticoid and so on. However the mechanisms regulating human alveolar type II epithelial cell replication upon cigarette smoke exposure remain poorly understood. To provide information on the influence of CSE on the repair capacity of the alveolar epithelium, I am interested in analyzing the effect of CSE on the proliferative response of alveolar type II epithelial cells. To document any protective role of retinoic acid (RA) to reverse the CSE effect, we are to examine the consequence of RA treatment on CSE-induced growth inhibition of type II epithelial cells。