Pulmonary Fibrosis, Emphysema, COPD Stem Cell Treatment

Stem Cell Therapy Pulmonary Fibrosis

 

Stem Cell Treatment for Pulmonary Fibrosis and COPD are now available at ASCI

Pulmonary fibrosis is the formation or development of excess fibrous connective tissue (fibrosis) in the lungs. It is also described as "scarring of the lung."

Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high Resolution CT will frequently demonstrate abnormalities.

Symptoms

Symptoms of pulmonary fibrosis are mainly:

  • Shortness of breath, particularly with exertion
  • Chronic dry, hacking coughing
  • Fatigue and weakness
  • Chest discomfort
  • Loss of appetite and rapid weight loss

Stem Cell Therapy Pulmonary Fibrosis and COPD

Possible Causes

Pulmonary fibrosis may be a secondary effect of other diseases. Most of these are classified as interstitial lung diseases. Examples include autoimmune disorders, viral infections or other microscopic injuries to the lung. However, pulmonary fibrosis can also appear without any known cause. In this case, it is termed "idiopathic". Most idiopathic cases are diagnosed as idiopathic pulmonary fibrosis. This is a diagnosis of exclusion of a characteristic set of histologic/pathologic features known as usual interstitial pneumonia (UIP). In either case, there is a growing body of evidence which points to a genetic predisposition in a subset of patients. For example, a mutation in Surfactant protein C (SP-C) has been found to exist in some families with a history of pulmonary fibrosis.

Diseases and conditions that may cause pulmonary fibrosis as a secondary effect include:

  • Inhalation of environmental and occupational pollutants, such as in asbestosis, silicosis and exposure to certain gases. Coal miners, ship workers and sand blasters among others are at higher risk. Hypersensitivity pneumonitis, most often resulting from inhaling dust contaminated with bacterial, fungal, or animal products.
  • Cigarette smoking can increase the risk or make the illness worse.
  • Some typical connective tissue diseases such as rheumatoid arthritis and Scleroderma. Other diseases that involve connective tissue, such as sarcoidosis and Wegener's granulomatosis.
  • Infections
  • Certain medications, e.g. amiodarone, bleomycin, busulfan, methotrexate, and nitrofurantoin
  • Radiation therapy to the chest.

Stem Cell Treatments for Pulmonary Fibrosis and COPD. Pulmonary Fibrosis and COPD and Stem Cell studies and protocols from the NIH:

Related Articles [Therapeutic effects and the underlying mechanism of umbilical cord-derived mesenchymal stem cells for bleomycin induced lung injury in rats]. Zhonghua Jie He He Hu Xi Za Zhi. 2013 Nov;36(11):808-13 Authors: Li YK, Wang H, Jiang CG, Huang H, Liu J, Wang YX, Xiao FJ, Wu ZZ, Xu ZJ Abstract OBJECTIVE: To study the efficacy of umbilical cord-derived mesenchymal stem cells (UC-MSCs) for bleomycin-induced pulmonary fibrosis in mice. METHODS: UC-MSCs were isolated from the umbilical cord after parental consent. One hundred C57BL/6 mice were randomly divided into 4 groups (12 of these for preliminary experiment). Mice in the control group (n = 20) were instilled with PBS via trachea and NS was injected via the tail vein after 3 days. Mice in the stem cell group (n = 20) were instilled with PBS via trachea and were injected with MSC via the tail vein after 3 days. Mice in the bleomycin group (n = 24) were instilled with bleomycin via trachea and NS was injected via the tail vein after 3 days. Mice in the bleomycin plus stem cell group (n = 24) were instilled with bleomycin via trachea and were injected with MSCs via the tail vein after 3 days. All of the mice were sacrificed at the 21(th) day, and the lungs were immediately fixed with 4% paraformaldehyde for 48 h, embedded in paraffin and sectioned at 5 µmol/L thickness. The sections were stained with hematoxylin and eosin (H&E) and Masson-trichrome. Histopathological scoring of pulmonary fibrosis was performed according to Ashcroft's method. The concentrations of matrix metalloproteinases-2 and tissue inhibitor of metalloproteinase-1were determined using immunohistochemistry. RESULTS: Compared with the bleomycin group, MSC transplantation significantly reduced pulmonary inflammation, fibrosis and deposition of collagen in the bleomycin plus stem cell group [(1.55 ± 0.51) vs (2.16 ± 0.77), and (1.45 ± 0.60) vs (2.32 ± 0.82), respectively, P < 0.05]. There was no difference between the control group and the stem cell group [(0.35 ± 0.49) vs (0.37 ± 0.50), P > 0.05]. The expression of MMP-2 in the bleomycin plus stem cell group was lower than the bleomycin group [(1.59 ± 0.59) vs (2.37 ± 0.68), P < 0.05], but there was no difference between the control group and the stem cell group [(0.80 ± 0.69) vs (0.84 ± 0.77), P > 0.05]. The expression of TIMP-1 in the bleomycin plus stem cell group was higher than the bleomycin group [(1.95 ± 0.58) vs (0.79 ± 0.71), P < 0.05], but there was no difference between the control group and the stem cell group [(1.10 ± 0.72) vs (1.32 ± 0.58), P > 0.05]. CONCLUSION: UC-MSC transplantation could relieve bleomycin-induced fibrosing alveolitis in mice. The mechanism might be related to the expression of MMP-2 and TIMP-1. UC-MSC had no effect on normal lungs. PMID: 24507390 [PubMed - indexed for MEDLINE]
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Related Articles The scaffold protein muscle A-kinase anchoring protein β orchestrates cardiac myocyte hypertrophic signaling required for the development of heart failure. Circ Heart Fail. 2014 Jul;7(4):663-72 Authors: Kritzer MD, Li J, Passariello CL, Gayanilo M, Thakur H, Dayan J, Dodge-Kafka K, Kapiloff MS Abstract BACKGROUND: Cardiac myocyte hypertrophy is regulated by an extensive intracellular signal transduction network. In vitro evidence suggests that the scaffold protein muscle A-kinase anchoring protein β (mAKAPβ) serves as a nodal organizer of hypertrophic signaling. However, the relevance of mAKAPβ signalosomes to pathological remodeling and heart failure in vivo remains unknown. METHODS AND RESULTS: Using conditional, cardiac myocyte-specific gene deletion, we now demonstrate that mAKAPβ expression in mice is important for the cardiac hypertrophy induced by pressure overload and catecholamine toxicity. mAKAPβ targeting prevented the development of heart failure associated with long-term transverse aortic constriction, conferring a survival benefit. In contrast to 29% of control mice (n=24), only 6% of mAKAPβ knockout mice (n=31) died in the 16 weeks of pressure overload (P=0.02). Accordingly, mAKAPβ knockout inhibited myocardial apoptosis and the development of interstitial fibrosis, left atrial hypertrophy, and pulmonary edema. This improvement in cardiac status correlated with the attenuated activation of signaling pathways coordinated by the mAKAPβ scaffold, including the decreased phosphorylation of protein kinase D1 and histone deacetylase 4 that we reveal to participate in a new mAKAP signaling module. Furthermore, mAKAPβ knockout inhibited pathological gene expression directed by myocyte-enhancer factor-2 and nuclear factor of activated T-cell transcription factors that associate with the scaffold. CONCLUSIONS: mAKAPβ orchestrates signaling that regulates pathological cardiac remodeling in mice. Targeting of the underlying physical architecture of signaling networks, including mAKAPβ signalosome formation, may constitute an effective therapeutic strategy for the prevention and treatment of pathological remodeling and heart failure. PMID: 24812305 [PubMed - indexed for MEDLINE]
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Related Articles Disease cell models - their use in industry TEDD workshop in Sion on 27 March 2014. Chimia (Aarau). 2014;68(6):446-8 Authors: Graf-Hausner U, Heinzelmann E Abstract On 27, March 2014, experts met at the first TEDD Workshop 2014, held at the HES-SO Valais/Wallis in Sion, to present innovative cell models for industrial applications. This was the first time that a TEDD event had been organized in French-speaking Switzerland and it offered local network partners an opportunity to showcase their research activities. PMID: 25198757 [PubMed - indexed for MEDLINE]
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