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1.
Rev Mal Respir ; 39(2): 79-83, 2022 Feb.
Artículo en Francés | MEDLINE | ID: mdl-35151521

RESUMEN

Pulmonary hypertension is a pulmonary circulation pathology characterized by remodelling and hyperreactivity of the pulmonary arteries. Vasodilatation/vasoconstriction balance is modified in favour of constriction via, among other things, the proliferation of smooth muscle cells and the development of endothelial dysfunction. In addition, the pulmonary arteries undergo modification of mechanical forces, inducing modified activation of stretch-activated channels (SAC) such as Piezo1 and TRPV4. These ionic channels are sensitive to stretch and their activation can induce various cellular physiological responses, which strongly contribute to development and continuation of the pathology.


Asunto(s)
Hipertensión Pulmonar , Humanos , Hipoxia/patología , Canales Iónicos , Miocitos del Músculo Liso , Arteria Pulmonar/patología , Circulación Pulmonar/fisiología , Canales Catiónicos TRPV
2.
Rev Mal Respir ; 37(3): 205-209, 2020 Mar.
Artículo en Francés | MEDLINE | ID: mdl-32151405

RESUMEN

Pulmonary hypertension is a severe multifactorial disease of the pulmonary circulation characterized by a progressive elevation in mean pulmonary arterial pressure (PAPm), leading to right ventricular failure and the death of the patient. Current therapies slow the progression of the disease but do not offer a cure. Nerve growth factor NGF is a growth factor playing a significant role in the pathophysiology of pulmonary hypertension, particularly in pulmonary arterial hyperreactivity, and the remodelling and inflammation of the pulmonary vasculature. Thus, targeting NGF may offer new therapeutic strategies in the treatment of this disease.


Asunto(s)
Hipertensión Pulmonar/genética , Factor de Crecimiento Nervioso/fisiología , Animales , Progresión de la Enfermedad , Expresión Génica , Humanos , Hipertensión Pulmonar/patología , Hipertensión Pulmonar/fisiopatología , Factor de Crecimiento Nervioso/genética , Circulación Pulmonar/genética
3.
Biochim Biophys Acta Mol Cell Biol Lipids ; 1862(9): 832-841, 2017 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-28504211

RESUMEN

Ecto-F1-ATPase is a complex related to mitochondrial ATP synthase which has been identified as a plasma membrane receptor for apolipoprotein A-I (apoA-I), the major protein of high-density lipoprotein (HDL), and has been shown to contribute to HDL endocytosis in several cell types. On hepatocytes, apoA-I binding to ecto-F1-ATPase stimulates extracellular ATP hydrolysis into ADP, which subsequently activates a P2Y13-mediated HDL endocytosis pathway. Interestingly, other mitochondrial proteins have been found to be expressed at the plasma membrane of several cell types. Among these, adenine nucleotide translocase (ANT) is an ADP/ATP carrier but its role in controlling extracellular ADP levels and F1-ATPase-mediated HDL endocytosis has never been investigated. Here we confirmed the presence of ANT at the plasma membrane of human hepatocytes. We then showed that ecto-ANT activity increases or reduces extracellular ADP level, depending on the extracellular ADP/ATP ratio. Interestingly, ecto-ANT co-localized with ecto-F1-ATPase at the hepatocyte plasma membrane and pharmacological inhibition of ecto-ANT activity increased extracellular ADP level when ecto-F1-ATPase was activated by apoA-I. This increase in the bioavailability of extracellular ADP accordingly translated into an increase of HDL endocytosis on human hepatocytes. This study thus uncovered a new location and function of ANT for which activity at the cell surface of hepatocytes modulates the concentration of extracellular ADP and regulates HDL endocytosis.


Asunto(s)
Adenosina Difosfato/metabolismo , Adenosina Trifosfato/metabolismo , Endocitosis/fisiología , Hepatocitos/metabolismo , Lipoproteínas HDL/metabolismo , Translocasas Mitocondriales de ADP y ATP/metabolismo , ATPasas de Translocación de Protón/metabolismo , Apolipoproteína A-I/metabolismo , Línea Celular , Línea Celular Tumoral , Membrana Celular/metabolismo , Células Hep G2 , Humanos , Proteínas Mitocondriales/metabolismo , Transducción de Señal/fisiología
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