Mitochondrial DNA 4977 bp deletion is a common phenomenon in hair and increases with age

Zheng, Yijie; Luo, Xiaowen; Zhu, Jü; Zhang, Xuan; Zhu, Yinting; Cheng, Huihua; Xia, Zhiqiu; Su, Na; Zhang, Nengpei; Zhou, Jian

doi:10.17305/bjbms.2012.2480

Cited by 22 publications

(16 citation statements)

References 11 publications

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“…It was identified that the incidence of mtDNA CD4977 in patients with presbycusis was significantly higher as compared with the age-matched normal hearing control individuals (67.82% vs. 8.42%, P=0.000). The presented PCR results are consistent with a previous study (7). Furthermore, the PCR products indicated the absence of mtDNA CD4977 in positive individuals verified by nested-PCR amplication (Fig.…”

supporting

confidence: 92%

“…Cochlea tissue is rich in mtDNA, which have a high probability of deletion. The deletions in mtDNA in cochlea tissue have been shown to include mtDNA 13162, 10422, 7663, 7436, 4989 and 4977 bp deletions, with the mtDNA CD4977 being the most common in cochlea tissue (7)(8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

“…Zheng et al (7), detected mtDNA CD4977 in the hair shaft of 90 selected cases (age ranges, 5 days-90 years) using PCR. The results indicated that the incidence of mtDNA CD4977 expression was 98.3% (89/90).…”

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confidence: 99%

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Association between the mitochondrial DNA 4977 common deletion in the hair shaft and hearing loss in presbycusis

Liu

Han

Wang

et al. 2014

Molecular Medicine Reports

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Abstract. The aim of the present study was to examine the role of the mitochondrial (mt) DNA common deletion (CD) 4977 (mtDNACD4977) in the hair shaft in patients with presbycusis. A total of 87 individuals with presbycusis and 95 normal-hearing controls were selected based on strict audiometric criteria. Nested polymerase chain reaction (PCR), sequencing and quantitative (q)PCR were used to examine the expression levels of mtDNA CD4977 in the hair shaft in presbycusis. Nested PCR of the hair shaft demonstrated that 8/95 cases with normal hearing were found to be positive for mtDNA CD4977 , as compared with 59/87 cases in the presbycusis group. The mtDNA CD4977 was positive in 22/43 cases with mild-to-moderate hearing loss, 25/31 cases with moderate-to-severe, severe hearing loss, and 12/13 cases with profound deafness. Statistically significant differences in mtDNA CD4977 expression were identified among all of the groups (P<0.001). The sequencing and qPCR assays demonstrated a trend towards an increase in the mean CD level of mtDNA CD4977 with a more severe hearing loss at 8 kHz (r=0.778, P<0.001) and all ranges of frequency (r=0.858, P<0.001). In conclusion, the present study demonstrates a correlation between mtDNA CD4977 in the human hair shaft and the severity of hearing loss in presbycusis.

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confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Association between the mitochondrial DNA 4977 common deletion in the hair shaft and hearing loss in presbycusis

Liu

Han

Wang

et al. 2014

Molecular Medicine Reports

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“…Since the relative proportion of mtDNA carrying the “common deletion” is known to be associated with increasing age and mortality [34, 35], we performed fixed-effect regression analysis to determine the association of both measurements of mtDNA copy number and mitochondrial injury with age. After correcting for the subset with measurements from both BA7 and BA8, we found that there was no association between the levels of mtDNA per cell and age (Fig.…”

Section: Resultsmentioning

confidence: 99%

Mitochondrial injury and cognitive function in HIV infection and methamphetamine use

Var

Day²,

Vitomirov³

et al. 2016

Aids

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Objective In this work we evaluated the association of human immunodeficiency virus (HIV) infection and methamphetamine (METH) use with mitochondrial injury in the brain and its implication on neurocognitive impairment. Design Mitochondria carry their genome (mtDNA) and play a critical role in cellular processes in the central nervous system. METH is commonly used in HIV-infected populations. HIV infection and METH use can cause damage to mtDNA and lead to neurocognitive morbidity. We evaluated HIV infection and METH use with mitochondrial injury in the brain. Methods We obtained white and gray matter from Brodmann’s areas (BA) BA7, BA8, BA9, and BA46 of a) HIV-infected individuals with history of past METH use (HIV+METH+, n=16), b) HIV-infected individuals with no history of past METH use (HIV+METH−, n=11), and c) HIV-negative controls (HIV−METH−, n=30). We used the “common deletion,” a 4,977 bp mutation, as a measurement of mitochondrial injury, and quantified levels of mtDNA and “common deletion” by droplet digital PCR, and evaluated in relation to neurocognitive functioning (Global Deficit Score [GDS]). Results Levels of mtDNA and mitochondrial injury were highest in white matter of BA46. A higher relative proportion of mtDNA carrying the “common deletion” was associated with lower GDS (p<0.01) in HIV+METH+ but higher GDS (p<0.01) in HIV+METH−. Conclusions Increased mitochondrial injury was associated with worse neurocognitive function in HIV+METH− individuals. Among HIV+METH+ individuals, an opposite effect was seen.

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“…Mitochondrial damage, particularly as a result of oxidative influences, can contribute to changes, such as deletions or mutations, in mitochondrial DNA. Analysis of hair fibers from participants ranging in age from 5 days to 91 years has revealed an increase in the incidence of a specific mitochondrial deletion over time, with 4,977 base-pair deletions by year 91 [32]. This rise in the frequency of base-pair deletions theoretically corresponds to a longer exposure to damaging effects like those from oxidation.…”

Section: Contributors To Hair Agingmentioning

confidence: 99%

Normal and Aging Hair Biology and Structure ‘Aging and Hair'

Goodier¹,

Hordinsky

2015

Alopecias - Practical Evaluation and Management

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Much like an individual's hairstyle, hair fibers along the scalp see a number of changes over the course of one's lifetime. As the decades pass, the shine and volume synonymous with youthful hair may give way to thin, dull, and brittle hair commonly associated with aging. These changes are a result of a compilation of genetic and environmental elements influencing the cells of the hair follicle, specifically the hair follicle stem cells and melanocytes. Telomere shortening, decrease in cell numbers, and particular transcription factors have all been implicated in this process. In turn, these molecular alterations lead to structural modifications of the hair fiber, decrease in melanin production, and lengthening of the telogen phase of the hair cycle. Despite this inevitable progression with aging, there exists an array of treatments such as light therapy, minoxidil, and finasteride which have been designed to mitigate the effects of aging, particularly balding and thinning hair. Although each works through a different mechanism, all aim to maintain or potentially restore the youthful quality of hair.

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Mitochondrial DNA 4977 bp deletion is a common phenomenon in hair and increases with age

Cited by 22 publications

References 11 publications

Association between the mitochondrial DNA 4977 common deletion in the hair shaft and hearing loss in presbycusis

Association between the mitochondrial DNA 4977 common deletion in the hair shaft and hearing loss in presbycusis

Mitochondrial injury and cognitive function in HIV infection and methamphetamine use

Normal and Aging Hair Biology and Structure ‘Aging and Hair'

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