Texas Medical Center

About: Texas Medical Center is a healthcare organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 2845 authors who have published 2394 publications receiving 79426 citations.

Cardiac myosin binding protein C regulates postnatal myocyte cytokinesis

Abstract: Homozygous cardiac myosin binding protein C-deficient (Mybpct/t) mice develop dramatic cardiac dilation shortly after birth; heart size increases almost twofold. We have investigated the mechanism of cardiac enlargement in these hearts. Throughout embryogenesis myocytes undergo cell division while maintaining the capacity to pump blood by rapidly disassembling and reforming myofibrillar components of the sarcomere throughout cell cycle progression. Shortly after birth, myocyte cell division ceases. Cardiac MYBPC is a thick filament protein that regulates sarcomere organization and rigidity. We demonstrate that many Mybpct/t myocytes undergo an additional round of cell division within 10 d postbirth compared with their wild-type counterparts, leading to increased numbers of mononuclear myocytes. Short-hairpin RNA knockdown of Mybpc3 mRNA in wild-type mice similarly extended the postnatal window of myocyte proliferation. However, adult Mybpct/t myocytes are unable to fully regenerate the myocardium after injury. MYBPC has unexpected inhibitory functions during postnatal myocyte cytokinesis and cell cycle progression. We suggest that human patients with homozygous MYBPC3-null mutations develop dilated cardiomyopathy, coupled with myocyte hyperplasia (increased cell number), as observed in Mybpct/t mice. Human patients, with heterozygous truncating MYBPC3 mutations, like mice with similar mutations, have hypertrophic cardiomyopathy. However, the mechanism leading to hypertrophic cardiomyopathy in heterozygous MYBPC3+/− individuals is myocyte hypertrophy (increased cell size), whereas the mechanism leading to cardiac dilation in homozygous Mybpc3−/− mice is primarily myocyte hyperplasia.

Antibody recognition of ragweed allergen Ra3: localization of the full profile of the continuous antigenic sites by synthetic overlapping peptides representing the entire protein chain.

Abstract: A comprehensive synthetic approach, for the localization of the full profile of the continuous antigenic sites on proteins, previously introduced by this laboratory, was applied here to localize the continuous antigenic sites of ragweed allergen, Ra3. The following 10 consecutive peptides, each comprising 15 residues (except for peptide 91-101) and overlapping each of its neighbors by 5 residues, were synthesized and purified: 1-15, 11-25, 21-35, 31-45, 41-55, 51-65, 61-75, 71-85, 81-95 and 91-101. Quantitative radiometric titrations of protein and peptide adsorbents were performed with 125I-labeled anti-Ra3 IgG antibodies from rabbit, outbred mouse and human antisera. The specificity of antibody binding to peptide adsorbents was confirmed by inhibition experiments. These studies established the full profile of antigenic (IgG-binding) sites of Ra3 and permitted comparison with the allergenic (IgE-binding) sites recently localized. It was found that the recognition by IgG antibodies was independent of the host species in which the antibodies were raised. Furthermore, the regions recognized by human IgE antibodies coincided with those recognized by IgG antibodies in three different species. Thus, Ra3 was found to have 4 continuous antigenic sites which occupy the same locations as the allergenic sites.

Differential Sensitivity of Estrogen Target Tissues: The Role of the Receptor*

Abstract: In this report, we describe the neuroendocrine features of the estrogen-implanted ovariectomized rat and define a number of estrogen-induced responses in these animals. We further demonstrate differential sensitivity to estradiol among several estrogen target tissues and investigate the role of the estrogen receptor in the mediation of this phenomenon. Ovariectomized rats implanted with a range of estradiol doses (1 μ-5 mg estradiol/capsule) provided a good experimental model for generation of dose response curves. These animals have serum estradiol levels that span the physiological range and that modulate numerous neuroendocrine endpoints. Using this animal model, dose response curves between estradiol and six estrogeninduced responses were generated. These responses included uterine wet and dry weight, negative and positive feedback of estrogen on serum LH levels, the LHRH content of neurosecretory terminals of the medial basal hypothalamus, and the size of the LHRH bolus released from the median emine...