Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease

Zhang, Chongxu; Cui, Tengjiao; Cai, Renzhi; Wangpaichitr, Medhi; Mirsaeidi, Mehdi; Jackson, Robert M.

doi:10.3390/cells9102331

Cited by 19 publications

(9 citation statements)

References 53 publications

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“…Once the micro-environment balance is disrupted, AEC senescence is initiated [ 34 ]. Cross-talk, such as that among IGF1, TGF-β, and Wnt, can also induce AECs senescence [ 35 – 37 ]. Blockade of a single signaling pathway can inhibit IPF to some extent; however, other pathways would be activated in compensation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of the IGF1 signaling pathway is involved in idiopathic pulmonary fibrosis induced by alveolar epithelial cell senescence and core fucosylation

Sun

Jing

Yang

et al. 2021

Aging

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Idiopathic pulmonary fibrosis (IPF) mainly occurs in elderly people over the age of sixty. IPF pathogenesis is associated with alveolar epithelial cells (AECs) senescence. Activation of PI3K/AKT signaling induced by insulin-like growth factor 1 (IGF1) participates in AEC senescence and IPF by releasing CTGF, TGF-β1, and MMP9. Our previous study demonstrated that core fucosylation (CF) modification, catalyzed by a specific core fucosyltransferase (FUT8) can regulate the activation of multiple signaling pathways, and inhibiting CF can alleviate pulmonary fibrosis in mice induced by bleomycin. However, whether CF is involved in IGF1-mediated AEC senescence in IPF remains unclear. In this study, we found that the IGF1/PI3K/AKT signaling pathway was activated in IPF lung tissue. Meanwhile, CF was present in senescent AECs. We also showed that IGF1 could induce AECs senescence with enhanced CF in vivo and in vitro . Inhibiting CF alleviated AECs senescence and pulmonary fibrosis induced by IGF1. In addition, activation of IGF1/PI3K/AKT signaling depends on CF. In conclusion, this study confirmed that CF is an important target regulating the IGF1 signaling pathway in AEC senescence and IPF, which might be a candidate target to treat IPF in the future.

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Section: Discussionmentioning

confidence: 99%

Regulation of the IGF1 signaling pathway is involved in idiopathic pulmonary fibrosis induced by alveolar epithelial cell senescence and core fucosylation

Sun

Jing

Yang

et al. 2021

Aging

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“…GHRH is secreted predominantly by the hypothalamus and stimulates the secretion of GH by the pituitary gland and regulates hepatic insulin-like growth factor-1 (IGF-1) production through the GH/hepatic IGF-1 axis ( 51 ). Other tissues, including the lungs also produce GHRH locally and express the receptor of GHRH (GHRHR) as well as the GHRHR splice variant 1 (SV1) ( 52 ).…”

Section: Central Endocrine (Hypothalamic and Pituitary) Hormonesmentioning

confidence: 99%

“…In normal mouse lung tissue, type 2 cells, club cells and fibroblasts, lymphocytes, and dendritic cells express GHRH ( 52 ). GHRH is involved in lung homeostasis, inflammation and fibrosis ( 51 ). Antagonists for GHRHR have anti-inflammatory, pro-apoptotic, anti-oxidative and anti-fibrotic effects in the lung.…”

Section: Central Endocrine (Hypothalamic and Pituitary) Hormonesmentioning

confidence: 99%

Interplay Between the Immune and Endocrine Systems in the Lung: Implications for TB Susceptibility

et al. 2022

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The role of the endocrine system on the immune response, especially in the lung, remains poorly understood. Hormones play a crucial role in the development, homeostasis, metabolism, and response to the environment of cells and tissues. Major infectious and metabolic diseases, such as tuberculosis and diabetes, continue to converge, necessitating the development of a clearer understanding of the immune and endocrine interactions that occur in the lung. Research in bacterial respiratory infections is at a critical point, where the limitations in identifying and developing antibiotics is becoming more profound. Hormone receptors on alveolar and immune cells may provide a plethora of targets for host-directed therapy. This review discusses the interactions between the immune and endocrine systems in the lung. We describe hormone receptors currently identified in the lungs, focusing on the effect hormones have on the pulmonary immune response. Altered endocrine responses in the lung affect the balance between pro- and anti-inflammatory immune responses and play a role in the response to infection in the lung. While some hormones, such as leptin, resistin and lipocalin-2 promote pro-inflammatory responses and immune cell infiltration, others including adiponectin and ghrelin reduce inflammation and promote anti-inflammatory cell responses. Furthermore, type 2 diabetes as a major endocrine disease presents with altered immune responses leading to susceptibility to lung infections, such as tuberculosis. A better understanding of these interactions will expand our knowledge of the mechanisms at play in susceptibility to infectious diseases and may reveal opportunities for the development of host-directed therapies.

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“…GH/IGF1 is centrally regulated by hypothalamic GH releasing hormone (GHRH), while GHRH and GHRH receptors are also expressed in peripheral tissue. The specific role of GHRH in the lung is discussed in the review by Zhang et al [ 5 ], which describes mechanisms of GHRH action on gene expression, mitochondria respiration, and intracellular signaling in lung development, growth, and repair in both cellular and animal models. The authors compare the effects of synthetic peptides mimicking GHRH action with endogenous GHRH, and analyze the effects of GHRH antagonists, which exert growth inhibitory effects in lung cancer cells in vitro and in vivo and act as anti-inflammatory agents.…”

mentioning

confidence: 99%