Mir200 Family Essay

Cystic fibrosis is an genetic disease that can cause bad damage to the lungs and other organs in the body. It is a common genetic (Gene) disease affecting to geriatric, (adults) young adults, or and kids. Now they’re still searching for a cure, but the only thing that is currently available is a donor’s lungs.

As you already know, Chronic Obstructive Pulmonary Disease (COPD), manifests itself when the passageway of air to the lungs is severely obstructed, thus preventing sufficient flow of oxygen into the bloodstream.1 The pathophysiology of COPD is a complex process that is the result of multiple airway diseases that simultaneously contribute to the impairment of airflow in the lungs.1 Specifically, the overlapping outcome of chronic bronchitis and emphysema is the pathogenesis of COPD.1 The risk factor for the COPD is influenced by the individual’s genetics, age, gender, exposure to air pollution, socioeconomic status, and the use of tobacco products.1 The use of tobacco products can increase the development of COPD.1 However, individuals that don’t smoke can also attain COPD.1 Therefore, COPD is not exclusive to individuals that smoke on a daily basis.1 In fact, genetics and the natural aging process plays a part in the development of pulmonary issues.1 For example, it has been proven that a deficiency in the alpha -1 antitrypsin gene is correlated with the development of COPD.1 The natural deterioration of lung tissue, coupled with the long term exposure to environmental elements, explains why the risk of attaining COPD increases as one progresses to the latter stages of their lives.1 In a healthy individual, goblet cells secrete about one liter of mucous that provides a moist surface over the lungs, trachea, and esophagus.1 The cilia on the pseuodocolumnar epithelial cells continuously sweep the mucus in the lungs in an upward motion.1 The cilia sweeps the mucosal trapped debris up, and removes pathogens and other foreign particles out the pulmonary tissue.1 In individuals with COPD, the pathogenesis of the disease creates structural modifications of the lung tissue, which result in deformed and nonfunctioning cilia.2 The lack of functioning cilia leads to the buildup of mucous, pathogens, and subsequent respiratory infections.2 Furthermore, the body tries to combat

Idiopathic pulmonary fibrosis is a horrible and ultimately fatal chronic lung disease in men and women. Characterized by irreversible loss of lung function, patients that are diagnosed are usually only given about 4 years to live. Although the cause of Idiopathic pulmonary fibrosis is still unknown, there are several risk factors involved. The symptoms of idiopathic pulmonary fibrosis are not specific, and are similar to many other types of pulmonary cardiac diseases. The majority of people with the disease have about a 6-month or more history of shortness of breath and/or nonproductive cough. About 5% of people with idiopathic pulmonary fibrosis do not have symptoms, and the disease is diagnosed when he or she is being examined for other medical

Idiopathic pulmonary fibrosis (IPF) is a fatal irreversible disease that severely diminishes lung function. IPF is part of a 200 + lung disease group known as interstitial lung diseases (ILD). The ILD group of diseases adversely affects the interstitium, which is the interstitial space between the lung tissue and air sacs. IPF is characterized by the scarring and honeycombing of the lung tissue and the accretion of fibrosis. The word 'idiopathic' is derived from the Greek word ‘idios’, which means 'of unknown cause' and aptly explain the status of the prognosis of this deadly disease. Some of the symptoms of IPF is shortness of breath (dyspnea), crackling sound in the lungs, finger clubbing and unrelenting dry cough.

Approximately 445 million dollars are spent on acute hospital stays for chronic obstructive pulmonary disease in Canada, not including ongoing care and prescription drugs (Leading Hospitalization Costs in Acute Inpatient Facilities in 2012–2013). A majority of this money is spent on treating patient’s symptoms, not their condition. A use for stem cells and regenerative medicine is to treat asthma, “Since it has been described that asthma is a disease of T cell hyperactivity and scarring, hMSCs may provide a viable multiaction therapeutic either directly through cell contact or through the production of bioactive factors,” (Bonfield). Despite asthma being a common condition, it follows people their entire life, and results in less productivity during a flare up. The use of stem cells to treat asthma may limit the prescriptions required to prevent a flare up, as well as allow easy breathing for asthma patients. Diabetes is a growing problem in society; however, stem cells may be able to correct the absence of insulin: “with in vivo virus-mediated expression of specific transcription factors in differentiated pancreatic exocrine cells resulting in the reprogramming of these cells into pancreatic β-like cells.” (Atala). While this new innovation could save the government money on insulin, it could also improve the quality of life for millions, and eradicate diabetes. Another application of stem cell research is to treat leukemia: “Another promising approach is the isolation and genetic modification of patients’ cells to target or enhance the efficacy of a cellular therapy. One example of this approach is the development of targeted immunotherapy for B-cell malignancies.” (Atala). This approach can counteract the irregularity of the blood cells, and provide a cure to this cancer. With the current knowledge of stem cells their curative potential seems

Idiopathic pulmonary fibrosis is a progressive lung disease of unknown cause that to date has no pharmacologic

enzymes are released to destroy foreign microbes and irritants such as cigarette smoke, air pollution,

Idiopathic pulmonary fibrosis (IPF) is a very devistating diagnosis that is associated with scarring and thickening of the lung tissue, making breathing a difficult task for patients (Bridges et al., 2014). Without a known cause, IPF progessively affects a patient’s lung fuction presenting as dyspnea, cough, and fatigue (Yount et al., 2016). This disease robs individuals of their quality of life, and their lifespan. Accoriding to (Bridges et al., 2014), an average lifespan of a patient after diagnosis is approximately three to five years. These patients lack independece in their normal everyday activities, their physical functioning declines, along with their respiratory function. Relief is sought through limited available interventions that

|Specific Purpose: |To inform readers on the causes, effects and treatments of lung cancer. |

Since the cloning of ABCC1 in the early 90s [14,15], progress has been made towards establishing a functional relationship between ABCC1 and CFTR. For example, functional complementation of dysfunctional CFTR by ABCC1 following chemotherapy that resulted in increased expression of ABCC1, was associated with improved lung function in a CF patient [12]. A study analyzing nasal epithelial cells in CF patients also showed that low ABCC1 transcript levels were associated with more

Many studies have been done regarding stem cells. One study looked at the role of the Wnt/β-catenin signaling pathway in the differentiation of mesenchymal stem cells into type II alveolar epithelial cells for the treatment of acute respiratory distress syndrome (ARDS). This study was done in mice with acute respiratory distress syndrome. β-catenin or GFP control were transfected into mice mesenchymal stem cells, and these mesenchymal stem cells were put into the trachea tissue of the mice. Several different assays and dyes, including immunofluorescent staining and Western blotting analysis, were used to assess the repair and differentiation that occurred. Results showed that MSCs in the lungs differentiated into type II alveolar epithelial cells and improved the permeability of the alveolar epithelia. This led to the conclusion that overexpression of β-catenin in mesenchymal stem cells can provide protection from epithelial damage and can help repair damage in mice with the syndrome through the activation of the Wnt/β-catenin pathway (Cai, et al.).

MDI exposure route in the occupational environment is thought to be mostly through inhalation and dermal contact {NIOSH, 2004 #145}. At room temperature, MDI is not volatile (with vapor pressure approximately at 10-5 mm Hg). During application, MDI is usually heated and/or aerosolized via a spray gun, thus generating repairable vapor and/or aerosols to allow inhalation into the lung. To mimic this MDI airway exposure route, we developed a nose-only aerosol exposure mouse model {Hettick, 2017 #179} to examine whether circulating mmu-miRs-183-5p, -206-3p, and -381-3p identified from MDI dermal exposure group could serve as potential biomarkers for the airway exposure route of MDI. Compare to mice exposed to house air only, mmu-miR-183-5p were upregulated 16.47-fold in serum collected at 4 hours (4h) after MDI-dust exposure and 41.57-fold in serum collected at 24 hours (24h)

Analysis of adipose derived induced pluripotent stem cells (iPSC’s) microRNA (miRNA) expression profile over multiple passages and pancreatic β-cell miRNA expression profile post differentiation from iPSC’s.

The hallmarks of a stem cell are its ability to self-renew as well as its ability to differentiate and assume almost any cell fate if given the appropriate cues known as pluripotency (ref). The differentiation of stem cells requires large and rapid changes in gene expression. miRNAs are well suited to carry out this task through their ability to simultaneously inhibit the translation of several target genes allowing for coordinated control of cellular processes{Bartel:2009fh}. Furthermore, miRNAs have been shown to regulate embryonic development in addition to their role in regulating stem cell fate{Stefani:2008bw}. Evidence for this comes from experimental studies where the overall function of the miRNA biogenesis pathway was evaluated through genetic deletion of the miRNA processing enzymes DICER, DGCR8, Drosha, and AGO2. DICER knockout mice die at early stages of embryogenesis and fail to express the stem cell marker Oct4 and primitive streak marker T (brachyury), which respectively indicate a loss of stem cells and arrested development during gastrulation{Bernstein:2003dp}. Furthermore, DICER-deficient mouse ES cells are viable but incapable of differentiation, showing severe proliferation defects{Kanellopoulou:2005kf, Murchison:2005fa}. Similarly, DGCR8 knockout mice arrest early in development{Wang:2007gb}. DGCR8-deficient mouse ES cells also exhibit a proliferation defect and cannot efficiently silence the ES cell program, although these defects are not as

Lesions of lungs comprise lymphangioleiomyomatosis (LAM) and multinodular multifocal pneumocystis hyperplasia (MMPH) which are present in round 1/3 mature women and rarely in males [1]. AML cells can migrate to the lungs causing proliferation of smooth muscle and progressive destruction of pulmonary parenchyma, resulting in a potentially fatal pulmonary disease known as lymphangioleiomyomatosis (LAM) [9].