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Article

Mitochondrial Ribosome Dysfunction in Human Alveolar Type II Cells in Emphysema

by
Loukmane Karim
1,2,
Chih-Ru Lin
1,2,
Beata Kosmider
1,2,3,
Gerard Criner
3,
Nathaniel Marchetti
3,
Sudhir Bolla
3,
Russell Bowler
4 and
Karim Bahmed
2,3,*
1
Department of Microbiology, Immunology, and Inflammation, Temple University, Philadelphia, PA 19140, USA
2
Center for Inflammation and Lung Research, Temple University, Philadelphia, PA 19140, USA
3
Department of Thoracic Medicine and Surgery, Temple University, Philadelphia, PA 19140, USA
4
Department of Medicine, National Jewish Health, Denver, CO 80206, USA
*
Author to whom correspondence should be addressed.
Biomedicines 2022, 10(7), 1497; https://doi.org/10.3390/biomedicines10071497
Submission received: 10 November 2021 / Revised: 17 April 2022 / Accepted: 26 April 2022 / Published: 24 June 2022
(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease)
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Abstract

Pulmonary emphysema is characterized by airspace enlargement and the destruction of alveoli. Alveolar type II (ATII) cells are very abundant in mitochondria. OXPHOS complexes are composed of proteins encoded by the mitochondrial and nuclear genomes. Mitochondrial 12S and 16S rRNAs are required to assemble the small and large subunits of the mitoribosome, respectively. We aimed to determine the mechanism of mitoribosome dysfunction in ATII cells in emphysema. ATII cells were isolated from control nonsmokers and smokers, and emphysema patients. Mitochondrial transcription and translation were analyzed. We also determined the miRNA expression. Decreases in ND1 and UQCRC2 expression levels were found in ATII cells in emphysema. Moreover, nuclear NDUFS1 and SDHB levels increased, and mitochondrial transcribed ND1 protein expression decreased. These results suggest an impairment of the nuclear and mitochondrial stoichiometry in this disease. We also detected low levels of the mitoribosome structural protein MRPL48 in ATII cells in emphysema. Decreased 16S rRNA expression and increased 12S rRNA levels were observed. Moreover, we analyzed miR4485-3p levels in this disease. Our results suggest a negative feedback loop between miR-4485-3p and 16S rRNA. The obtained results provide molecular mechanisms of mitoribosome dysfunction in ATII cells in emphysema.
Keywords: alveolar type II cells; emphysema; mitochondria; mitoribosome; lung alveolar type II cells; emphysema; mitochondria; mitoribosome; lung

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MDPI and ACS Style

Karim, L.; Lin, C.-R.; Kosmider, B.; Criner, G.; Marchetti, N.; Bolla, S.; Bowler, R.; Bahmed, K. Mitochondrial Ribosome Dysfunction in Human Alveolar Type II Cells in Emphysema. Biomedicines 2022, 10, 1497. https://doi.org/10.3390/biomedicines10071497

AMA Style

Karim L, Lin C-R, Kosmider B, Criner G, Marchetti N, Bolla S, Bowler R, Bahmed K. Mitochondrial Ribosome Dysfunction in Human Alveolar Type II Cells in Emphysema. Biomedicines. 2022; 10(7):1497. https://doi.org/10.3390/biomedicines10071497

Chicago/Turabian Style

Karim, Loukmane, Chih-Ru Lin, Beata Kosmider, Gerard Criner, Nathaniel Marchetti, Sudhir Bolla, Russell Bowler, and Karim Bahmed. 2022. "Mitochondrial Ribosome Dysfunction in Human Alveolar Type II Cells in Emphysema" Biomedicines 10, no. 7: 1497. https://doi.org/10.3390/biomedicines10071497

APA Style

Karim, L., Lin, C.-R., Kosmider, B., Criner, G., Marchetti, N., Bolla, S., Bowler, R., & Bahmed, K. (2022). Mitochondrial Ribosome Dysfunction in Human Alveolar Type II Cells in Emphysema. Biomedicines, 10(7), 1497. https://doi.org/10.3390/biomedicines10071497

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