Tachykinins and neurokinin receptors in bone marrow functions: neural-hematopoietic link

Klassert, Tilman E.; Patel, Shyam A.; Rameshwar, Pranela

doi:10.2147/jrlcr.s6509

Cited by 5 publications

(2 citation statements)

References 117 publications

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“…Through a diminishing inclusion that interferes with regular homeostatic tissue maintenance and regeneration response, senescence is likely to play a significant role in the pathophysiology of senescence in many tissues. Companion cells in the BM microenvironment control HSC function [ 19 , 20 ]. HSCs mediate ongoing blood cell production throughout the organism's lifespan by their protected capacity to self-renew to sustain the stem cell pool and differentiate to give rise to all terminally differentiated blood cells.…”

Section: Introductionmentioning

confidence: 99%

A state-of-the-art review on the MicroRNAs roles in hematopoietic stem cell aging and longevity

et al. 2023

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Aging is a biological process determined through time-related cellular and functional impairments, leading to a decreased standard of living for the organism. Recently, there has been an unprecedented advance in the aging investigation, especially the detection that the rate of senescence is at least somewhat regulated via evolutionarily preserved genetic pathways and biological processes. Hematopoietic stem cells (HSCs) maintain blood generation over the whole lifetime of an organism. The senescence process influences many of the natural features of HSC, leading to a decline in their capabilities, independently of their microenvironment. New studies show that HSCs are sensitive to age-dependent stress and gradually lose their self-renewal and regeneration potential with senescence. MicroRNAs (miRNAs) are short, non-coding RNAs that post-transcriptionally inhibit translation or stimulate target mRNA cleavage of target transcripts via the sequence-particular connection. MiRNAs control various biological pathways and processes, such as senescence. Several miRNAs are differentially expressed in senescence, producing concern about their use as moderators of the senescence process. MiRNAs play an important role in the control of HSCs and can also modulate processes associated with tissue senescence in specific cell types. In this review, we display the contribution of age-dependent alterations, including DNA damage, epigenetic landscape, metabolism, and extrinsic factors, which affect HSCs function during aging. In addition, we investigate the particular miRNAs regulating HSCs senescence and age-associated diseases. Graphical Abstract

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Section: Introductionmentioning

confidence: 99%

A state-of-the-art review on the MicroRNAs roles in hematopoietic stem cell aging and longevity

et al. 2023

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“…It is possible that neurochemicals liberated by these nerve endings in response to chemical stimuli or injury may have a role in fibrogenesis. Tachykinins (ubiquitously expressed ancient neuropeptides with diverse function, such as substance P) are liberated by these nerve endings and the corresponding specific receptors are expressed on marrow cells [ 72 , 73 ]. Uncertainties exist about their exact role in marrow function and fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Fibrosis and bone marrow: understanding causation and pathobiology

Ghosh,

Shome,

Kulkarni

et al. 2023

J Transl Med

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Bone marrow fibrosis represents an important structural change in the marrow that interferes with some of its normal functions. The aetiopathogenesis of fibrosis is not well established except in its primary form. The present review consolidates current understanding of marrow fibrosis. We searched PubMed without time restriction using key words: bone marrow and fibrosis as the main stem against the terms: growth factors, cytokines and chemokines, morphology, megakaryocytes and platelets, myeloproliferative disorders, myelodysplastic syndrome, collagen biosynthesis, mesenchymal stem cells, vitamins and minerals and hormones, and mechanism of tissue fibrosis. Tissue marrow fibrosis-related papers were short listed and analysed for the review. It emerged that bone marrow fibrosis is the outcome of complex interactions between growth factors, cytokines, chemokines and hormones together with their facilitators and inhibitors. Fibrogenesis is initiated by mobilisation of special immunophenotypic subsets of mesenchymal stem cells in the marrow that transform into fibroblasts. Fibrogenic stimuli may arise from neoplastic haemopoietic or non-hematopoietic cells, as well as immune cells involved in infections and inflammatory conditions. Autoimmunity is involved in a small subset of patients with marrow fibrosis. Megakaryocytes and platelets are either directly involved or are important intermediaries in stimulating mesenchymal stem cells. MMPs, TIMPs, TGF-β, PDGRF, and basic FGF and CRCXL4 chemokines are involved in these processes. Genetic and epigenetic changes underlie many of these conditions.

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Human acute myeloid leukemia cells express Neurokinin-1 receptor, which is involved in the antileukemic effect of Neurokinin-1 receptor antagonists

et al. 2018

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The substance P/neurokinin-1 receptor system has been implicated in tumor cell proliferation. Neurokinin-1 receptor has been identified in different solid tumors but not frequently in hematopoietic malignant cells. We investigated the presence of the Neurokinin-1 receptor in acute myeloid leukemia cell lines (KG-1 and HL-60), demonstrating that acute myeloid leukemia cell lines overexpress the truncated Neurokinin-1 receptor isoform compared with lymphocytes from healthy donors. Using the MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) method, we demonstrated that substance P induced cell proliferation in both acute myeloid leukemia cell lines. We also observed that four different Neurokinin-1 receptor antagonists (L-733,060, L-732,138, CP 96-345 and aprepitant) elicited inhibition of acute myeloid leukemia cell growth lines in a concentration-dependent manner, while growth inhibition was only marginal in lymphocytes; the specific antitumor action of Neurokinin-1 receptor antagonists occurs via the Neurokinin-1 receptor, and leukemia cell death is due to apoptosis. Finally, administration of high doses of daily intraperitoneal fosaprepitant to NOD scid gamma mice previously xenografted with the HL60 cell line increased the median survival from 4 days (control group) to 7 days (treated group) (p = 0.059). Taken together, these findings suggest that Neurokinin-1 receptor antagonists suppress leukemic cell growth and may be considered to be potential antitumor drugs for the treatment of human acute myeloid leukemia.

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Tachykinins and neurokinin receptors in bone marrow functions: neural-hematopoietic link

Cited by 5 publications

References 117 publications

A state-of-the-art review on the MicroRNAs roles in hematopoietic stem cell aging and longevity

A state-of-the-art review on the MicroRNAs roles in hematopoietic stem cell aging and longevity

Fibrosis and bone marrow: understanding causation and pathobiology

Human acute myeloid leukemia cells express Neurokinin-1 receptor, which is involved in the antileukemic effect of Neurokinin-1 receptor antagonists

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