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Compositions and methods for treating pulmonary fibrosis

A technique for pulmonary fibrosis, a composition, applied in the field of morbidity and mortality composition, capable of solving the problem of not 'reversing' fibrosis, etc.

Active Publication Date: 2020-03-31
THE ARIZONA BOARD OF REGENTS ON BEHALF OF THE UNIV OF ARIZONA +1
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

No available therapy that can 'reverse' fibrosis

Method used

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  • Compositions and methods for treating pulmonary fibrosis
  • Compositions and methods for treating pulmonary fibrosis
  • Compositions and methods for treating pulmonary fibrosis

Examples

Experimental program
Comparison scheme
Effect test

example 1

[0277] Example 1: IPF lung myofibroblasts exhibit senescence and apoptosis resistance.

[0278] Materials and methods

[0279] Reagents: Porcine platelet-derived TGF-beta1 from R&D Systems (Minneapolis, MN). Staurosporine from LC Laboratories (Woburn, MA). Antibodies against: actin (clone AC-15) and alpha-tubulin (clone B-5-1-2) from Sigma (St. Louis, MO); a-SMA (clone ASM-1) from American Research Products (Belmont, MA); cleaved caspase 3, cleaved PARP and Bcl-2 from cell signaling Cell Signaling (Boston, MA); Nox4 and Ki67 from Novus Biologicals (Littleton, CO); and p21, Col1A1 and nuclear fibrils Lamin A / C from Santa Cruz Biotechnology (Dallas, TX). Antibodies against p16INK4a were from Santa Cruz Biotechnology and BD Biosciences (San Jose, CA). Antibodies against GAPDH were from Abbott and Cell Signaling. All other reagents were purchased from Sigma Corporation (St. Louis, MO) unless otherwise noted.

[0280] Lung Histology and Immunohistochemical Staining: Paraffin...

example 2

[0287] Example 2: Aged mice show impaired regression of fibrosis and accumulation of senescent myofibroblasts.

[0288] Materials and methods

[0289] Materials and methods are described above.

[0290] detect H 2 O 2 . Determination of extracellular H from cultured cells 2 O 2 freed. Cell numbers were normalized by DAPI (Fluorescent Cell Count Normalization Kit; Marker Gene Technologies).

[0291] result

[0292] Figure 1 shows that aged mice exhibit a lack of regression of bleomycin-induced lung injury compared to young mice. Aged mice exhibited the persistence of myofibroblasts in fibrotic areas of the lung 2 months after injury as compared to young mice with regressed fibrosis, as determined by αSMA immunohistochemical (IHC) staining. figure 2 showed that fibroblasts isolated from young and old mice exhibited p16 induction in response to transient injury in young mice that was in old mice with persistent fibrosis continuous. Fibroblasts isolated from damaged lun...

example 3

[0294] Example 3: Accumulated senescent myofibroblasts in aged mice show resistance to apoptosis.

[0295] Materials and methods

[0296] Materials and methods are described above.

[0297] result

[0298] Consistent with the human IPF data, Figure 4A and 4B It is shown that lung tissue sections from aged mice after lung injury show lower levels of apoptosis (TUNEL+ cells) in areas of fibrosis compared to young mice. Fibroblasts isolated from aged mice exhibited resistance to apoptosis, and fewer apoptotic cells were resistant to the apoptosis-inducing agent staurosporine ( Figure 4A ). Consistent with the acquisition of an anti-apoptotic phenotype, the lungs of aged mice exhibited elevated Bcl-2 levels ( Figure 4B ).

[0299] Taken together, these results demonstrate that fibrosis that does not resolve upon aging is associated with the acquisition of a senescent and apoptosis-resistant myofibroblast phenotype.

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Abstract

Inhibition of the expression and / or function of nicotinamide phosphoribosyltransferase (NAMPT) can reduce, prevent or reverse the pathophysiological vascular changes associated with the onset and progression of Pulmonary Fibrosis. Compositions and methods to inhibit the expression and function of NAMPT for treating and preventing Pulmonary Fibrosis in a subject in need are provided. The compositions and methods are useful for the modulation of pathophysiological processes that contribute to the development and progression of Pulmonary Fibrosis by reducing lung inflammation, aberrant myofibroblast accumulation and deposition of collagen in fibrotic foci.

Description

[0001] CROSS-REFERENCE TO RELATED APPLICATIONS [0002] This application claims priority to US Provisional Application No. 62 / 485,863, filed April 14, 2017, entitled "Methods for treating fibrosis," the contents of which are incorporated by reference in their entirety way to incorporate. [0003] Sequence Listing Reference [0004] The Sequence Listing, created on April 16, 2018 and having a size of 17,398 bytes, is hereby incorporated by reference as submitted as a text file named "UA_17_154_PCT_ST25.txt". [0005] Statement Regarding Federally Funded Research or Development [0006] This invention was made with US Government support under Grant No. 1IK2 BXOOI477-01AI awarded by the Veterans Administration. The United States Government has certain rights in this invention. technical field [0007] The field of the invention relates generally to compositions and methods for reducing morbidity and mortality associated with pulmonary fibrosis. Background technique ...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): C12N15/113C12N15/115A61K31/4545A61P11/00C07K16/28
CPCA61K31/4545A61P11/00C07K2317/76C07K16/40C07K2317/55A61K31/4439A61K31/444A61K31/713A61K9/0019
Inventor J·G·N·加西亚L·赫克
Owner THE ARIZONA BOARD OF REGENTS ON BEHALF OF THE UNIV OF ARIZONA
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