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Biomedical subjects

Janice Liebler

Publications and source records attributed to Janice Liebler.

2 recordsLinked to original sources

Developmental pathways and specification of intrapulmonary stem cells.

Tissues have the capacity to maintain a homeostatic balance between wear-and-tear and regeneration. Repair of non-lethal injury also activates cell proliferation to repopulate the injured sites with appropriate cell types and to restore function. Although controversial, the source of the material appears to be at least partly from pools of unique, multipotent stem cells that reside in specialized locations referred to as "niches." Molecular interactions between the niche and the intracellular factors within stem cells are crucial in maintaining stem cell functions, particularly the balance between self-renewal and differentiation. Many of the mediators of the stem cell-niche interactions are similar or identical to those that control developmental pathways during organogenesis. In this review, we present a systematic discussion and evaluation of the relevant literature with a focused emphasis on three primary signaling pathways, WNT, SHH and BMP with potentially overlapping roles during both development and stem cell maintenance.

Humans↗

Modulation of ion conductance and active transport by TGF-beta 1 in alveolar epithelial cell monolayers.

Transforming growth factor-beta1 (TGF-beta 1) may be a critical mediator of lung injury and subsequent remodeling during recovery. We evaluated the effects of TGF-beta 1 on the permeability and active ion transport properties of alveolar epithelial cell monolayers. Rat alveolar type II cells plated on polycarbonate filters in defined serum-free medium form confluent monolayers and acquire the phenotypic characteristics of alveolar type I cells. Exposure to TGF-beta 1 (0.1-100 pM) from day 0 resulted in a concentration- and time-dependent decrease in transepithelial resistance (Rt) and increase in short-circuit current (Isc). Apical amiloride or basolateral ouabain on day 6 inhibited Isc by 80 and 100%, respectively. Concurrent increases in expression of Na+-K+-ATPase alpha 1- and beta 1-subunits were observed in TGF-beta 1-treated monolayers. No change in the alpha-subunit of the rat epithelial sodium channel (alpha-rENaC) was seen. Exposure of confluent monolayers to TGF-beta 1 from day 4 resulted in an initial decrease in Rt within 6 h, followed by an increase in Isc over 72-96 h. These results demonstrate that TGF-beta 1 modulates ion conductance and active transport characteristics of the alveolar epithelium, associated with increased Na+-K+-ATPase, but without a change in alpha-rENaC.

Amiloride↗