Molecular mechanisms underlying the induction of neuronal Na channel expression by growth factors.

1995 ◽  
Author(s):  
Gary R. Fanger
Keyword(s):  
Growth Factors ◽  
Molecular Mechanisms ◽  
Na Channel ◽  
Channel Expression

Angiogenesis: molecular mechanisms and functional interactions

2003 ◽  
Vol 89 (01) ◽  
pp. 190-197 ◽  
Author(s):  
Georg Breier ◽  
Hellmut Augustin
Keyword(s):  
Growth Factors ◽  
Research Program ◽  
Tumor Invasion ◽  
Molecular Mechanisms ◽  
Precursor Cells ◽  
Invasion And Metastasis ◽  
Angiogenic Growth Factors ◽  
Cell Contacts ◽  
Functional Interactions ◽  
Biannual Meeting

SummaryThe German Priority Research Program “Angiogenesis” (www.angiogenese.de) hosts a biannual meeting in the Kloster Seeon in Southern Germany. The 2nd Kloster Seeon Meeting “Angiogenesis: Molecular Mechanisms and Functional Interactions” was held in September 2002. It included sessions on hypoxia, the biology of endothelial precursor cells, angiogenic growth factors including VEGFs, the angiopoietins, ephrins, and FGFs, mechanisms of vascular sprouting and cell-cell contacts during angiogenesis, angiogenic signaling, lymphangiogenesis, angiogenesis during tumor invasion and metastasis, and on novel angiomanipulatory therapies. This report summarizes the key findings reported during the platform presentations of the meeting.

Amiloride sensitive Na+ channel expression in the ileum after total colectomy in rats

1995 ◽  
Vol 108 (4) ◽  
pp. A982
Author(s):  
K. Koyama ◽  
I. Sasaki ◽  
Y. Funayama ◽  
H. Naito ◽  
T. Tsuchiya ◽  
...  
Keyword(s):  
Total Colectomy ◽  
Na Channel ◽  
Channel Expression

scholarly journals Bone remodeling stages under physiological conditions and glucocorticoid in excess: Focus on cellular and molecular mechanisms

2021 ◽  
Vol 12 (2) ◽  
pp. 212-227
Author(s):  
V. V. Povoroznyuk ◽  
N. V. Dedukh ◽  
M. A. Bystrytska ◽  
V. S. Shapovalov
Keyword(s):  
Growth Factors ◽  
Bone Resorption ◽  
Signaling Pathways ◽  
Bone Remodeling ◽  
Molecular Mechanisms ◽  
Signaling Molecules ◽  
Physiological Conditions ◽  
Bone Cell Differentiation ◽  
Repressive Effect

This review provides a rationale for the cellular and molecular mechanisms of bone remodeling stages under physiological conditions and glucocorticoids (GCs) in excess. Remodeling is a synchronous process involving bone resorption and formation, proceeding through stages of: (1) resting bone, (2) activation, (3) bone resorption, (4) reversal, (5) formation, (6) termination. Bone remodeling is strictly controlled by local and systemic regulatory signaling molecules. This review presents current data on the interaction of osteoclasts, osteoblasts and osteocytes in bone remodeling and defines the role of osteoprogenitor cells located above the resorption area in the form of canopies and populating resorption cavities. The signaling pathways of proliferation, differentiation, viability, and cell death during remodeling are presented. The study of signaling pathways is critical to understanding bone remodeling under normal and pathological conditions. The main signaling pathways that control bone resorption and formation are RANK / RANKL / OPG; M-CSF – c-FMS; canonical and non-canonical signaling pathways Wnt; Notch; MARK; TGFβ / SMAD; ephrinB1/ephrinB2 – EphB4, TNFα – TNFβ, and Bim – Bax/Bak. Cytokines, growth factors, prostaglandins, parathyroid hormone, vitamin D, calcitonin, and estrogens also act as regulators of bone remodeling. The role of non-encoding microRNAs and long RNAs in the process of bone cell differentiation has been established. MicroRNAs affect many target genes, have both a repressive effect on bone formation and activate osteoblast differentiation in different ways. Excess of glucocorticoids negatively affects all stages of bone remodeling, disrupts molecular signaling, induces apoptosis of osteocytes and osteoblasts in different ways, and increases the life cycle of osteoclasts. Glucocorticoids disrupt the reversal stage, which is critical for the subsequent stages of remodeling. Negative effects of GCs on signaling molecules of the canonical Wingless (WNT)/β-catenin pathway and other signaling pathways impair osteoblastogenesis. Under the influence of excess glucocorticoids biosynthesis of biologically active growth factors is reduced, which leads to a decrease in the expression by osteoblasts of molecules that form the osteoid. Glucocorticoids stimulate the expression of mineralization inhibitor proteins, osteoid mineralization is delayed, which is accompanied by increased local matrix demineralization. Although many signaling pathways involved in bone resorption and formation have been discovered and described, the temporal and spatial mechanisms of their sequential turn-on and turn-off in cell proliferation and differentiation require additional research.

scholarly journals Mechanisms and regulatory factors of endometrial neovascularization

2022 ◽  
pp. 26-33
Author(s):  
V. M. Chertok ◽  
A. E. Kotsyuba ◽  
I. A. Khramova
Keyword(s):  
Growth Factors ◽  
Menstrual Cycle ◽  
Formation Process ◽  
Molecular Mechanisms ◽  
Focal Point ◽  
Regulatory Factors ◽  
Vascular Walls

Cellular-molecular mechanisms and factors, regulating uterus vascularization are also a focal point ensuring reproduction processes. In the process of angiogenesis endothelium expresses a number of receptors of growth factors and ligands which control main stages of the cellular makeup during vascular walls formation process. It in turn supports proliferation and reparation of the endometrium during menstrual cycle and prepares for the implantation and placentation.

scholarly journals The molecular mechanisms of multidrug resistance of human glioblastomas

2021 ◽  
Vol 67 (1) ◽  
pp. 20-28
Author(s):  
Alexandr Chernov ◽  
Irina Baldueva ◽  
Tatyana Nekhaeva ◽  
Elvira Galimova ◽  
Diana Alaverdian ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Drug Resistance ◽  
Transcription Factors ◽  
Growth Factors ◽  
Multidrug Resistance ◽  
Tumor Suppressor Genes ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Polymorphic Variants ◽  
Signal Transduction Proteins

In review discusses the phenomenon of drug resistance of GB in the context of the expression of ABC family transporter proteins and the processes of proliferation, angiogenesis, recurrence and death. The emphasis is on the identifying for molecular targets among growth factors, receptors, signal transduction proteins, microRNAs, transcription factors, proto-oncogenes, tumor suppressor genes and their polymorphic variants (SNPs) for the development and creation of targeted anticancer drugs.

scholarly journals MicroRNA-204 Is Necessary for Aldosterone-Stimulated T-Type Calcium Channel Expression in Cardiomyocytes

2018 ◽  
Vol 19 (10) ◽  
pp. 2941 ◽  
Author(s):  
Riko Koyama ◽  
Tiphaine Mannic ◽  
Jumpei Ito ◽  
Laurence Amar ◽  
Maria-Christina Zennaro ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Molecular Mechanisms ◽  
Calcium Currents ◽  
Neonatal Rat ◽  
Messenger Rnas ◽  
Screening Assay ◽  
Rat Cardiomyocytes ◽  
Ventricular Cardiomyocytes ◽  
Channel Expression ◽  
Beating Frequency

Activation of the mineralocorticoid receptor (MR) in the heart is considered to be a cardiovascular risk factor. MR activation leads to heart hypertrophy and arrhythmia. In ventricular cardiomyocytes, aldosterone induces a profound remodeling of ion channel expression, in particular, an increase in the expression and activity of T-type voltage-gated calcium channels (T-channels). The molecular mechanisms immediately downstream from MR activation, which lead to the increased expression of T-channels and, consecutively, to an acceleration of spontaneous cell contractions in vitro, remain poorly investigated. Here, we investigated the putative role of a specific microRNA in linking MR activation to the regulation of T-channel expression and cardiomyocyte beating frequency. A screening assay identified microRNA 204 (miR-204) as one of the major upregulated microRNAs after aldosterone stimulation of isolated neonatal rat cardiomyocytes. Aldosterone significantly increased the level of miR-204, an effect blocked by the MR antagonist spironolactone. When miR-204 was overexpressed in isolated cardiomyocytes, their spontaneous beating frequency was significantly increased after 24 h, like upon aldosterone stimulation, and messenger RNAs coding T-channels (CaV3.1 and CaV3.2) were increased. Concomitantly, T-type calcium currents were significantly increased upon miR-204 overexpression. Specifically repressing the expression of miR-204 abolished the aldosterone-induced increase of CaV3.1 and CaV3.2 mRNAs, as well as T-type calcium currents. Finally, aldosterone and miR-204 overexpression were found to reduce REST-NRSF, a known transcriptional repressor of CaV3.2 T-type calcium channels. Our study thus strongly suggests that miR-204 expression stimulated by aldosterone promotes the expression of T-channels in isolated rat ventricular cardiomyocytes, and therefore, increases the frequency of the cell spontaneous contractions, presumably through the inhibition of REST-NRSF protein.

scholarly journals Fetal hyperinsulinemia increases farnesylation of p21 Ras in fetal tissues

2001 ◽  
Vol 281 (2) ◽  
pp. E217-E223 ◽  
Author(s):  
Elizabeth Stephens ◽  
Patti J. Thureen ◽  
Marc L. Goalstone ◽  
Marianne S. Anderson ◽  
J. Wayne Leitner ◽  
...  
Keyword(s):  
Growth Factors ◽  
Molecular Mechanisms ◽  
Fetal Liver ◽  
White Blood Cells ◽  
Causative Factor ◽  
Ras Proteins ◽  
Direct Infusion ◽  
Fetal Tissues ◽  
P21 Ras

Even though the role of fetal hyperinsulinemia in the pathogenesis of fetal macrosomia in patients with overt diabetes and gestational diabetes mellitus seems plausible, the molecular mechanisms of action of hyperinsulinemia remain largely enigmatic. Recent indications that hyperinsulinemia “primes” various tissues to the mitogenic influence of growth factors by increasing the pool of prenylated Ras proteins prompted us to investigate the effect of fetal hyperinsulinemia on the activitiy of farnesyltransferase (FTase) and the amounts of farnesylated p21 Ras in fetal tissues in the ovine experimental model. Induction of fetal hyperinsulinemia by direct infusion of insulin into the fetus and by either fetal or maternal infusions of glucose resulted in significant increases in the activity of FTase and the amounts of farnesylated p21 Ras in fetal liver, skeletal muscle, fat, and white blood cells. An additional infusion of somatostatin into hyperglycemic fetuses blocked fetal hyperinsulinemia and completely prevented these increases, specifying insulin as the causative factor. We conclude that the ability of fetal hyperinsulinemia to increase the size of the pool of farnesylated p21 Ras may prime fetal tissues to the action of other growth factors and thereby constitute one mechanism by which fetal hyperinsulinemia could induce macrosomia in diabetic pregnancies.

scholarly journals Ion Channels: New Actors Playing in Chemotherapeutic Resistance

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 376 ◽  
Author(s):  
Philippe Kischel ◽  
Alban Girault ◽  
Lise Rodat-Despoix ◽  
Mohamed Chamlali ◽  
Silviya Radoslavova ◽  
...  
Keyword(s):  
Ion Channels ◽  
Molecular Mechanisms ◽  
Early Stage ◽  
Breast Cancers ◽  
Altered Expression ◽  
Acquired Drug Resistance ◽  
Therapeutic Modalities ◽  
Channel Expression ◽  
Systemic Agents ◽  
Resistance To Chemotherapy

In the battle against cancer cells, therapeutic modalities are drastically limited by intrinsic or acquired drug resistance. Resistance to therapy is not only common, but expected: if systemic agents used for cancer treatment are usually active at the beginning of therapy (i.e., 90% of primary breast cancers and 50% of metastases), about 30% of patients with early-stage breast cancer will have recurrent disease. Altered expression of ion channels is now considered as one of the hallmarks of cancer, and several ion channels have been linked to cancer cell resistance. While ion channels have been associated with cell death, apoptosis and even chemoresistance since the late 80s, the molecular mechanisms linking ion channel expression and/or function with chemotherapy have mostly emerged in the last ten years. In this review, we will highlight the relationships between ion channels and resistance to chemotherapy, with a special emphasis on the underlying molecular mechanisms.

scholarly journals Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Dehai Xian ◽  
Jing Song ◽  
Lingyu Yang ◽  
Xia Xiong ◽  
Rui Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Molecular Mechanisms ◽  
Capillary Tube ◽  
Proteolytic Enzymes ◽  
Skin Tumor ◽  
Antioxidant Systems ◽  
Antiangiogenic Factors ◽  
And Oxidative Stress

Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.

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