#Stem cell treatment lung disease Activator
#Stem cell treatment lung disease plus

differentiation is regulated by the bone morphogenetic protein (BMP) signaling pathway. During lung homeostasis, AT2 cells also function as self-renewing alveolar progenitor cells, in addition to differentiating into AT1 cells, which facilitate gas exchange. Alveolar type II cells (AT2) cells secrete surfactants essential for alveolar function, such as surfactant protein C (pro-SP-C). Schematic of putative progenitors of the alveolar epithelium. KRT, cytokeratin ASCL1, achaete-scute homolog 1 CGRP, calcitonin gene-related peptide FOX, forkhead box protein CFTR, cystic fibrosis transmembrane conductance regulator PGP9.5, protein gene product 9.5 RGS13, regulator of G protein signalling 13 SCGB1A1, secretoglobin family 1A member 1/club cell secretory protein/club cell 10 kDa protein secretory club cells SP-C, surfactant protein C MUC, mucin TFCP2, transcription factor CP2 SSEA-1, stage specific embryonic antigen 1. 5) BCs can also give rise to self-renewing neuroendocrine cells as well as brush cells and ionocytes. 4) If BCs are ablated, club-like cells (CCs) have been demonstrated to dedifferentiate to renew BCs. Alveolar type II and bronchiolar cells are additional contributions from CCs. 3) club-like cells (CCs) share a common pathway with BCs when differentiating into MCCs but can also renew the MCCs through a goblet cell (GC) intermediate.

#Stem cell treatment lung disease Activator

Other identified pathways that induce this lineage relationship include signal transducer and activator of transcription 3 (STAT3)/IL-6 or inhibitory miR-449. 2) A subset of these BCs that display intracellular Notch commit to a secretory cell lineage while low-level c- myb expression in the same population will differentiate to preciliated and multiciliated cells (MCCs) subsequently. 1) Basal cells (BC) self-renew and are capable of giving rise to all cell types present on the surface airway epithelium through an intermediate BC precursor. Illustration of basal stem cells and their putative differentiated progeny in the human lung. BV, blood vessel BASC, bronchioalveolar stem cell. Progenitor/stem cells (marked in red and listed) reside in their respective local niches, and these environments enable them to maintain their stem/progenitor properties and control their ability to differentiate into various progeny cell types. These include the submucosal gland (SMG) ducts in the proximal trachea, basal cells within intercartilaginous zones of the trachea and primary bronchi, neuroepithelial bodies (NEBs) in the intralobar bronchi and bronchioles, and the bronchioalveolar duct junction (BADJ) and alveolar spaces within the alveoli. Distinct region-specific stem/progenitor cell niches are thought to exist along the proximal-distal axis of the airway.

#Stem cell treatment lung disease plus

The lung can be divided into three major levels of conducting airways (the trachea, bronchi, and bronchioles) plus the gas-exchanging alveoli. Illustration of putative stem/progenitor cells and their niches in the adult murine lung. As our capacity to model the human lung evolves, so will our understanding of lung regeneration and our ability to target endogenous stem cells as a therapeutic approach for lung disease.Īirway epithelium basal cells cell therapy differentiation pulmonary neuroendocrine cells. These advancements include novel lineage-traced animal models and single-cell RNA sequencing of human airway cells, which have provided critical information on the stem cell subtypes, transition states, identifying cell markers, and intricate pathways that commit a stem cell to differentiate or to maintain plasticity. Additionally, we highlight the recent breakthroughs that have increased our understanding of these cell types. In this review, we intend to discuss the known stem/progenitor cell populations, their relative differences between rodents and humans, their roles in chronic lung disease, and their therapeutic prospects. Progress toward the development of strategies to regenerate the adult lung by either in vivo or ex vivo targeting of endogenous stem cells or pluripotent stem cell derivatives is limited by our fundamental lack of understanding of the mechanisms controlling human lung development, the precise identity and function of human lung stem and progenitor cell types, and the genetic and epigenetic control of human lung fate. The ability to replace defective cells in an airway with cells that can engraft, integrate, and restore a functional epithelium could potentially cure a number of lung diseases.