Pulmonary administration of integrin-nanoparticles regenerates collapsed alveoli

Horiguchi, Michiko; Kojima, Hisako; Sakai, Hitomi; Kubo, Hiroshi; Yamashita, Chikamasa

doi:10.1016/j.jconrel.2014.05.050

Cited by 17 publications

(19 citation statements)

References 23 publications

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“…Pulmonary administration of ATRA repaired the collapsed alveoli of emphysema model mice by alveolar repairing. 6) PPARβ/δ is one of the nuclear receptors that can be activated by ATRA. Stimulation of PPARβ/δ affects many cellular process, including glucose metabolism, fatty acid metabolism, and keratinocyte, 19,20) adipocyte and sebocyte differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…5) We recently reported that ATRA induced the differentiation of human lung alveolar epithelial type 2 progenitor cells (AEPCs) into alveolar type II epithelial (AT-II) cells, which secrete surfactant protein, surfactant protein A (SP-A), and repair the alveoli of emphysema model mouse. 6) ATRA has been used as an alternative therapy for acute promyelocytic leukemia (APL), a specific acute myeloid leukemia subtype characterized by a chromosomal translocation t (15; 17) involving the retinoid acid receptor (RAR) α gene on chromosome 17 and the promyelocytic gene on chromosome 15. ATRA can induce the differentiation of APL blasts both in vitro and in vivo via stimulation of RARα.…”

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confidence: 99%

“…For evaluation of the expression level of AT-II cells and the lung sections and average of the distance between alveolar walls, 6 weeks old ICR male mice (Sankyo Labo Service Corporation, Inc., Tokyo, Japan) received 7.5 U/head porcine pancreatic elastase (Wako Pure Chemical Industries, Ltd.) once a week and then 4.05 U/head elastase twice a week dissolved in 50 µL saline delivered transpulmonarily allowed previous method. 6) For evaluation of the tissue elastance and respiratory function, 6 weeks old ICR male mice (Sankyo Labo Service Corporation, Inc.) received 4.05 U/head elastase dissolved in 50 µL saline twice a week delivered transpulmonarily allowed previous method.…”

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Pulmonary Administration of GW0742, a High-Affinity Peroxisome Proliferator-Activated Receptor Agonist, Repairs Collapsed Alveoli in an Elastase-Induced Mouse Model of Emphysema

Ozawa

Horiguchi

Akita

et al. 2016

Biological & Pharmaceutical Bulletin

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Pulmonary emphysema is a disease in which lung alveoli are irreversibly damaged, thus compromising lung function. Our previous study revealed that all-trans-retinoic acid (ATRA) induces the differentiation of human lung alveolar epithelial type 2 progenitor cells and repairs the alveoli of emphysema model mice. ATRA also reportedly has the ability to activate peroxisome proliferator-activated receptor (PPAR) β/δ. A selective PPARβ/δ ligand has been reported to induce the differentiation of human keratinocytes during wound repair. Here, we demonstrate that treatment using a high-affinity PPARβ/δ agonist, GW0742, reverses the lung tissue damage induced by elastase in emphysema-model mice and improves respiratory function. Mice treated with elastase, which collapsed their alveoli, were then treated with either 10% dimethyl sulfoxide (DMSO) in saline (control group) or GW0742 (1.0 mg/kg twice a week) by pulmonary administration. Treatment with GW0742 for 2 weeks increased the in vivo expression of surfactant proteins A and D, which are known alveolar type II epithelial cell markers. GW0742 treatment also shortened the average distance between alveolar walls in the lungs of emphysema model mice, compared with a control group treated with 10% DMSO in saline. Treatment with GW0742 for 3 weeks also improved tissue elastance (cm H 2 O/mL), as well as the ratio of the forced expiratory volume in the first 0.05 s to the forced vital capacity (FEV 0.05/ FVC). In each of these experiments, GW0742 treatment reversed the damage caused by elastase. In conclusion, PPARβ/δ agonists are potential therapeutic agents for pulmonary emphysema.

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Pulmonary Administration of GW0742, a High-Affinity Peroxisome Proliferator-Activated Receptor Agonist, Repairs Collapsed Alveoli in an Elastase-Induced Mouse Model of Emphysema

Ozawa

Horiguchi

Akita

et al. 2016

Biological & Pharmaceutical Bulletin

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“…A melting curve was generated at the end of every run to ensure product uniformity. The primer sequences of ADRP [16], PPARβ/δ [17] and GAPDH [3] are shown in (Table 1). GAPDH was used as reference gene.…”

Section: Reverse Transcription and Rt-pcrmentioning

confidence: 99%

“…AT-II cells have the ability to proliferate and differentiate into alveolar type I epithelial cells through the alveolar repair process. ATRA treatment also significantly improves the CT values of normal mice and elastasetreated mice, a mouse model of emphysema [3]. However, the detailed mechanisms underlying ATRA-induced differentiation of human AEPCs remain unclear.…”

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Peroxisome Proliferator-Activated Receptor β/δ Stimulation Induces the Differentiation of Human Alveolar Epithelial Progenitor Cell

Ozawa¹,

Horiguchi²,

Akita³

et al. 2016

Insights Chest Dis

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Tel: +81 4 7121 3691 Fax: +81 4 7121 3622 factor. Human AEPCs are purified from adult human lung using two selection procedures. The first is a negative selection that removes hematopoietic cells using an autoMACS Separator with anti-human CD45 antibody-coated microbeads. The second is a positive selection that picks out lung stem cells using FACSAria with anti-human pro-SP-C (an alveolar cell marker) and antihuman CD90 (a mesenchymal stem cell marker) antibodies [2].Recently, we showed that all-trans-retinoic acid (ATRA), a metabolite of retinol (vitamin A), has the ability to induce the differentiation of human AEPCs to AT-II cells. AT-II cells have the ability to proliferate and differentiate into alveolar type I epithelial cells through the alveolar repair process. ATRA treatment also significantly improves the CT values of normal mice and elastasetreated mice, a mouse model of emphysema [3]. However, the detailed mechanisms underlying ATRA-induced differentiation of human AEPCs remain unclear.ATRA can activate two nuclear receptors: nuclear retinoic acid IntroductionChronic obstructive pulmonary disease (COPD), the fourth leading cause of death according to a report released by World Health Organization in 2005, is an increasing global health problem. COPD includes three pathological manifestations: chronic obstructive bronchitis, mucus plugging, and pulmonary emphysema. Pulmonary emphysema is a disease in which the lung's gas-exchange structures, the alveoli, are irreversibly destroyed, causing the patient to die of compromised lung function unless a transplant is provided. The causes of COPD have not been clearly defined. However, many lipid mediators, inflammatory peptides, reactive oxygen and nitrogen species, chemokines, cytokines, and growth factors have been implicated in alveolar destruction [1].Human alveolar epithelial progenitor cells (AEPCs) have been shown to self-renew. They also can differentiate into alveolar type II epithelial (AT-II) cells upon stimulation with a growth Peroxisome Proliferator-Activated Receptor β/δ Stimulation Induces the Differentiation of Human Alveolar Epithelial Progenitor Cell AbstractPulmonary emphysema is a disease in which alveoli in the lung are irreversibly destroyed, compromising lung function. All-trans-retinoic acid (ATRA) reportedly repairs the alveoli of emphysema model mice. In addition, ATRA can activate two nuclear receptors, nuclear retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) β/δ. Both of these receptors induce differentiation in many different cell types. In this study, PPARβ/δ stimulation is shown to induce differentiation of human alveolar epithelial progenitor cells into alveolar type II epithelial (AT-II) cells. PPARβ/δ activation also stimulates the expression of adipose differentiation-related protein mRNA in human alveolar epithelial progenitor cells. These data suggest that PPARβ/δ selective agonists could differentiate human alveolar epithelial progenitor cells without cytotoxic of ATRA derived from stimu...

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Impact of Nanotechnology on the Realm of Stem Cells and Regenerative Medicine

2022

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The intersection of very different, yet complementary fields, stem cells and nanotechnology, has led to the opening of new horizons in the area of research, giving new hopes, better strategies, and a boost to regenerative medicine, nanotherapeutics, and tissue engineering. Harnessing the stem cell's ability to self‐renew and differentiate into specific types of functional cells and the unique physico‐chemical properties of the nanomaterials, researchers have optimized the interactions of these with the biological milieu to overcome the hurdles of conventional cell‐based therapies. Here, we highlight and outline various types of nanomaterials and their well‐established significance in redefining the future of human medicine through influencing stem cell research targeting illness of important human organs.

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Pulmonary administration of integrin-nanoparticles regenerates collapsed alveoli

Cited by 17 publications

References 23 publications

Pulmonary Administration of GW0742, a High-Affinity Peroxisome Proliferator-Activated Receptor Agonist, Repairs Collapsed Alveoli in an Elastase-Induced Mouse Model of Emphysema

Pulmonary Administration of GW0742, a High-Affinity Peroxisome Proliferator-Activated Receptor Agonist, Repairs Collapsed Alveoli in an Elastase-Induced Mouse Model of Emphysema

Peroxisome Proliferator-Activated Receptor β/δ Stimulation Induces the Differentiation of Human Alveolar Epithelial Progenitor Cell

Impact of Nanotechnology on the Realm of Stem Cells and Regenerative Medicine

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