Connective tissue growth factor is responsible for transforming growth factor-beta-induced peritoneal mesothelial cell apoptosis. 2006

Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
Department of Medicine, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, SAR, China. ccszeto@cuhk.edu.hk

BACKGROUND Previous studies found that transforming growth factor-beta (TGF-beta) induces mesothelial production of connective tissue growth factor (CTGF), which may be downstream mediators of TGF-beta. Since high dose TGF-beta induces apoptosis of peritoneal mesothelial cells (PMC), we study the effect of CTGF blockade in the system of TGF-beta-induced PMC apoptosis. METHODS We examined the effect of TGF-W in primary culture of rat peritoneal mesothelial cells (PMC). PMC apoptosis was studied by flow cytometry. The effect of CTGF was blocked by antibody and short-interfering RNA (siRNA). Expression of apoptotic gene was studied by real-time polymerase chain reaction. RESULTS In cultured unstimulated rat PMC, there is a low but definite incidence of spontaneous apoptosis. Stimulation with TGF-beta 50 pg/ml induces an upregulation of apoptotic gene BAX expression and a downregulation of anti-apoptotic gene BCL-2L expression, and a 4-fold increase in PMC apoptosis. The effect of TGF-beta-induced PMC apoptosis was partly prevented by antibody against CTGF, and completely abolished by CTGF-specific siRNA, while CTGF-blockade by siRNA had no effect on PMC necrosis. CTGF silencing by siRNA prevented the down-regulation of BCL-2L expression induced by TGF-beta, had no effect on the BAX expression. CONCLUSIONS Our results indicate that CTGF is an important downstream mediator of TGF-beta-induced PMC apoptosis.

UI MeSH Term Description Entries
D007249 Inflammation A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. Innate Inflammatory Response,Inflammations,Inflammatory Response, Innate,Innate Inflammatory Responses
D010537 Peritoneum A membrane of squamous EPITHELIAL CELLS, the mesothelial cells, covered by apical MICROVILLI that allow rapid absorption of fluid and particles in the PERITONEAL CAVITY. The peritoneum is divided into parietal and visceral components. The parietal peritoneum covers the inside of the ABDOMINAL WALL. The visceral peritoneum covers the intraperitoneal organs. The double-layered peritoneum forms the MESENTERY that suspends these organs from the abdominal wall. Parietal Peritoneum,Peritoneum, Parietal,Peritoneum, Visceral,Visceral Peritoneum,Parametrium,Parametriums
D004847 Epithelial Cells Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells. Adenomatous Epithelial Cells,Columnar Glandular Epithelial Cells,Cuboidal Glandular Epithelial Cells,Glandular Epithelial Cells,Squamous Cells,Squamous Epithelial Cells,Transitional Epithelial Cells,Adenomatous Epithelial Cell,Cell, Adenomatous Epithelial,Cell, Epithelial,Cell, Glandular Epithelial,Cell, Squamous,Cell, Squamous Epithelial,Cell, Transitional Epithelial,Cells, Adenomatous Epithelial,Cells, Epithelial,Cells, Glandular Epithelial,Cells, Squamous,Cells, Squamous Epithelial,Cells, Transitional Epithelial,Epithelial Cell,Epithelial Cell, Adenomatous,Epithelial Cell, Glandular,Epithelial Cell, Squamous,Epithelial Cell, Transitional,Epithelial Cells, Adenomatous,Epithelial Cells, Glandular,Epithelial Cells, Squamous,Epithelial Cells, Transitional,Glandular Epithelial Cell,Squamous Cell,Squamous Epithelial Cell,Transitional Epithelial Cell
D005355 Fibrosis Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. Cirrhosis,Fibroses
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D015536 Down-Regulation A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins. Receptor Down-Regulation,Down-Regulation (Physiology),Downregulation,Down Regulation,Down-Regulation, Receptor
D015854 Up-Regulation A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins. Receptor Up-Regulation,Upregulation,Up-Regulation (Physiology),Up Regulation
D016212 Transforming Growth Factor beta A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins. Bone-Derived Transforming Growth Factor,Platelet Transforming Growth Factor,TGF-beta,Milk Growth Factor,TGFbeta,Bone Derived Transforming Growth Factor,Factor, Milk Growth,Growth Factor, Milk
D017207 Rats, Sprague-Dawley A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company. Holtzman Rat,Rats, Holtzman,Sprague-Dawley Rat,Rats, Sprague Dawley,Holtzman Rats,Rat, Holtzman,Rat, Sprague-Dawley,Sprague Dawley Rat,Sprague Dawley Rats,Sprague-Dawley Rats
D017209 Apoptosis A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis

Related Publications

Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
May 2006, American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
February 2010, Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
January 2008, The international journal of biochemistry & cell biology,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
October 1999, FASEB journal : official publication of the Federation of American Societies for Experimental Biology,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
December 1999, European journal of pharmacology,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
June 2004, Experimental eye research,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
September 2008, Journal of cellular physiology,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
August 2019, Scientific reports,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
May 1996, The American journal of pathology,
Cheuk-Chun Szeto, and Kai-Ming Chow, and Ka-Bik Lai, and Carol Yi-Ki Szeto, and Bonnie Ching-Ha Kwan, and Philip Kam-Tao Li
November 2001, Current opinion in rheumatology,
Copied contents to your clipboard!