Defective FGFR2 Signaling in the Small Airway Basal Progenitor Cells in COPD

Status: Active_not_recruiting
Location: See location...
Study Type: Observational
SUMMARY

Early changes associated with the development of smoking-induced diseases, e.g., COPD and lung cancer (the two commonest causes of death in U.S.) are often characterized by abnormal airway epithelial differentiation. Airway basal cells (BC) are stem/progenitor cells necessary for generation of differentiated airway epithelium. Based on our preliminary observations on SAE BC cells and FGFR2 signaling, we hypothesized that suppression of FGFR2 signaling in the SAE BC stem/progenitor cells by cigarette smoking renders these cells less potent in generating and maintaining normally differentiated SAE, shifting these cells towards a COPD associated phenotype. To test this, SAE basal cells will be isolated from cultured cells obtained through bronchoscopic brushings and analyzed through in vitro assays for their stem/progenitor capacities.

Eligibility
Participation Requirements
Sex: All
Minimum Age: 18
Healthy Volunteers: t
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• Must be capable of providing informed consent

• Males and females, age 18 or older

• Nonsmoking, matched with other groups by age, sex, ethnic/racial group

• Good overall health without history of chronic lung disease, including asthma, and without recurrent or recent (within 3 months) acute pulmonary disease

• Normal physical examination

• Normal routine laboratory evaluation, including general hematologic studies, general serologic/ immunologic studies, general biochemical analyses, and urine analysis

• Negative HIV serology

• Normal chest X-ray (PA and lateral)

• Normal electrocardiogram

• Females - not pregnant

• No history of allergies to medications to be used in the bronchoscopy procedure

• Not taking any medications relevant to lung disease or having an effect on the airway epithelium

• Willingness to participate in the study

Locations
United States
New York
Weill Cornell Medicine
New York
Time Frame
Start Date: 2014-07
Completion Date: 2025-12
Participants
Target number of participants: 120
Treatments
Healthy nonsmokers
n=20 for Aim 1 n=20 for Aim 2~Aim 1.To determine whether BC from the SAE of COPD smokers have reduced capacity to generate normally differentiated SAE, e.g initiate airway branching and repair in response to injury in vitro but generate airway epithelium with the phenotype similar to that present in SAE of COPD smokers in vivo.~Aim 2.To test the hypothesis that FGFR2 signaling is necessary for normal SAE BC stem cell function and suppression of FGFR2 caused by inhibitors and smoking associated factors (EGF and TGF- beta)leads an altered stem cell functional phenotype similar to SAE BC from COPD smokers with reduced capacity as characterized by Aim 1.
Healthy smokers
n=20- for Aim 1 n=20 for Aim 3~Aim 1.To determine whether BC from the SAE of COPD smokers have reduced capacity to generate normally differentiated SAE, e.g initiate airway branching and repair in response to injury in vitro but generate airway epithelium with the phenotype similar to that present in SAE of COPD smokers in vivo.~Aim 3.To assess the hypothesis that increasing FGFR2 signaling and suppressing smoking induced EGF receptors and TGF-beta pathways will restore the FGFR2 expression and normalize the capacity of SAE BC stem cells to generate and maintain normally differentiated SAE.
COPD smokers
n=20- for Aim 1 n=20 for Aim 3~Aim 1.To determine whether BC from the SAE of COPD smokers have reduced capacity to generate normally differentiated SAE, e.g initiate airway branching and repair in response to injury in vitro but generate airway epithelium with the phenotype similar to that present in SAE of COPD smokers in vivo.~Aim 3.To assess the hypothesis that increasing FGFR2 signaling and suppressing smoking induced EGF receptors and TGF-beta pathways will restore the FGFR2 expression and normalize the capacity of SAE BC stem cells to generate and maintain normally differentiated SAE.
Authors
Renat Shaykhiev, Robert Kaner, Ronald G Crystal
Sponsors
Leads: Weill Medical College of Cornell University
Collaborators: National Heart, Lung, and Blood Institute (NHLBI)

This content was sourced from clinicaltrials.gov