ABSTRACT
We examined the localization of the pituitary adenylate cyclase-activating peptide (PACAP) receptor (PAC1-R) and its mRNA with immunocytochemistry and in situ hybridization, respectively. PAC1-R immunoreactivity and its transcript were detected in both chromaffin cells and ganglion cells but not detected in the adrenal cortex. In addition, strong PAC1-R immunoreactivity was found beneath the plasma membrane of the immunoreactive medullary cells. Electron microscopic immunocytochemistry revealed that PAC1-R was predominantly expressed in adrenaline-containing cells. This report supports the notion that PACAP is an activator and modulator of catecholamine secretion as well as synthesis in the adrenal medulla.
Subject(s)
Adrenal Medulla/metabolism , Neuropeptides/metabolism , Receptors, Pituitary Hormone/metabolism , Adrenal Medulla/ultrastructure , Animals , Male , Pituitary Adenylate Cyclase-Activating Polypeptide , RNA, Messenger/metabolism , Rats , Rats, Sprague-Dawley , Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide , Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide , Receptors, Pituitary Hormone/genetics , Signal Transduction/physiologyABSTRACT
Ultraviolet light (UV)-induced DNA repair during myeloid leukemic cell differentiation was examined. Human myeloid leukemic cells could be induced to differentiate in vitro into mature cells by various chemical inducers that lost their proliferating potencies. In spite of decrease of proliferation capacity, almost all these terminally differentiated myeloid leukemic cells invariably showed UV-induced unscheduled DNA synthesis (UDS) at low energy of UV irradiation (3-5J/m2). This indicated that the terminally differentiated myeloid leukemic cells are functionally quite different from mature granulocytes in chronic myeloid leukemia (CML) or in normal peripheral blood. In HL-60 cells, UV-survival was enhanced in the process of differentiation induced by 1.25% DMSO or 0.6 mM sodium n-butyrate. The degree of enhancement of UV-survival was correlated with the increased amount of UDS. The process of myeloid leukemic cell differentiation which is completed without loss of capacity performing repair DNA synthesis was one of the characteristics of the terminally differentiated myeloid leukemic cells induced by chemical inducers in vitro and this function may support the hypothesis that DNA breaking and rejoining are involved in a mechanism of cytodifferentiation.
Subject(s)
DNA Repair/radiation effects , DNA, Neoplasm/radiation effects , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics , Leukemia, Promyelocytic, Acute/genetics , Cell Differentiation/radiation effects , Humans , Tumor Cells, Cultured , Ultraviolet RaysSubject(s)
Cell Separation , Plateletpheresis , Thrombocytosis/therapy , Humans , Male , Middle Aged , Thrombocytosis/bloodABSTRACT
Myotendon junctions in the rectus abdominis muscles of bull frogs were examined by the fixation combination of tannic acid and glutaraldehyde using electron microscopy. The features observed on myotendon junctions were the following: (1) There were many deep invaginations of muscle cell membrane at the end of the muscle fibers. Terminal thin filaments of myofibrils were attached to the electron-dense layer lining under the muscle cell membrane on the lateral walls of invaginations. (2) The basement membrane covering the muscle cell membrane was thicker in the invaginations than on the other sites of muscle fibers. (3) Collagen fibers in the invaginations gradually tapered off toward the bottom of the invaginations. But it was not seen that the collagen fibers were attached to both the basement membrane and cell membrane of muscle cells. (4) On the observations using the tannic acid-glutaraldehyde fixation, it was clearly seen that the microfibrils extend from the outer leaflets of the cell membrane to the collagen fibers in invaginations via the basement membrane. It was concluded that the myofibrils might be fastened to the collagen fibers of the tendon by the intermediates of the microfibrils.
