Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss

Kamogashira, Teru; Fujimoto, Chisato; Yamasoba, Tatsuya

doi:10.1155/2015/617207

Cited by 153 publications

(148 citation statements)

References 100 publications

Supporting

Mentioning

135

Contrasting

Unclassified

Order By: Relevance

“…Induction of apoptosis is a mechanism involved in the action of AMPs (18)(19)(20). Dual staining with AV and PI demonstrated that rates of apoptosis were significantly ROS, typically regarded as toxic products of cellular metabolism, are able to function as signaling molecules that regulate a number of physiological processes (21). ROS are important in the induction of apoptosis in physiological and pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Bovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells

Meng

et al. 2016

Oncology Letters

View full text Add to dashboard Cite

Abstract. Bovine lactoferricin P13 (LfcinB-P13) is a peptide derived from LfcinB. In the present study, the effect of LfcinB-P13 on the human liver cancer cell line SMMC7721 was investigated in vitro and in vivo. The results of the present study indicate that LfcinB-P13 significantly decreased SMMC7721 cell viability in vitro (P=0.032 vs. untreated cells), while exhibiting low cytotoxicity in the wild-type liver cell line L02. In addition, the rate of apoptosis in SMMC7721 cells was significantly increased following treatment with 40 and 60 µg/ml LfcinB-P13 (P=0.0053 vs. the control group), which was associated with an increase in the level of reactive oxygen species (ROS) and the activation of caspase-3 and -9. Furthermore, ROS chelation led to the suppression of LfcinB-P13-mediated caspase-3 and -9 activation in SMMC7721 cells. LfcinB-P13 was demonstrated to markedly inhibit tumor growth in an SMMC7721-xenograft nude mouse model. The results of the present study indicate that LfcinB-P13 is a novel candidate therapeutic agent for the treatment of liver cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Bovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells

Meng

et al. 2016

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…Acoustic trauma damages sensory cells, neurons, and support cells as well as disrupts the microcirculation in the cochlea (Canlon, 1987; Canlon, 1988; Hultcrantz et al, 1987; Kamogashira et al, 2015; Kujawa et al, 2015; Liberman et al, 2015; Ohlemiller et al, 2007; Shi, 2009; Shi et al, 2007; Wang et al, 2002; Yoshida et al, 1999). Increased vascular permeability, reduced circulation (ischemia), aggregation of leukocytes, and injury to endothelial cells are frequently seen in loud sound exposed animals (Goldwyn et al, 1997; Hultcrantz et al, 1987; Lamm et al, 1999; Quirk et al, 1992; Scheibe et al, 1993; Seidman et al, 1999; Shi et al, 2007; Suzuki et al, 2002).…”

Section: Intrastrial Fluid-blood Barrier and Hearing Disordersmentioning

confidence: 99%

“…A variety of drugs, including antibacterial aminoglycoside antibiotics such as gentamicin and amikacin, anticancer agents such as cisplatin, carboplatin, nedaplatin, and oxaliplatin as well as loop diuretics such as furosemide, have side effects that damage the sense of hearing or balance in humans and animals (Ding et al, 2012; Kamogashira et al, 2015; Karasawa et al, 2011; Oishi et al, 2012; Rybak et al, 2007; Schacht et al, 2012). Recent research shows the intrastrial fluid–blood barrier might be a main port of entry for certain ototoxic drugs from the blood into cochlear fluids (Adamson, 2009; Dai et al, 2008; Laurell et al, 2000; Wang et al, 2009).…”

Section: Intrastrial Fluid-blood Barrier and Hearing Disordersmentioning

confidence: 99%

Pathophysiology of the cochlear intrastrial fluid-blood barrier (review)

2016

View full text Add to dashboard Cite

The blood-labyrinth barrier (BLB) in the stria vascularis is a highly specialized capillary network that controls exchanges between blood and the intrastitial space in the cochlea. The barrier shields the inner ear from blood-born toxic substances and selectively passes ions, fluids, and nutrients to the cochlea, playing an essential role in the maintenance of cochlear homeostasis. Anatomically, the BLB is comprised of endothelial cells (ECs) in the strial microvasculature, elaborated tight and adherens junctions, pericytes (PCs), basement membrane (BM), and perivascular resident macrophage-like melanocytes (PVM/Ms), which together form a complex “cochlear-vascular unit” in the stria vascularis. Physical interactions between the ECs, PCs, and PVM/Ms, as well as signaling between the cells, is critical for controlling vascular permeability and providing a proper environment for hearing function. Breakdown of normal interactions between components of the BLB is seen in a wide range of pathological conditions, including genetic defects and conditions engendered by inflammation, loud sound trauma, and ageing. In this review, we will discuss prevailing views of the structure and function of the strial cochlear-vascular unit (also referred to as the “intrastrial fluid-blood barrier”). We will also discuss the disrupted homeostasis seen in a variety of hearing disorders. Therapeutic targeting of the strial barrier may offer opportunities for improvement of hearing health and amelioration of auditory disorders.

show abstract

“…Increasing number of studies demonstrated that hearing impairment following cochlear damage due to noise trauma, drug ototoxicity or age-related cochlear degeneration is directly linked to a common pathogenesis involving the formation of ROS [38][39][40][41]. In this way, some studies demonstrated that age-related loss of cochlear hair cells was accelerated in Sod1 mutant mice [42], whereas guinea pig overexpressing catalase in their cochlea significantly protected hair cells and hearing thresholds after ototoxic treatment [43].…”

Section: Mitochondrial Ros In Hearing Lossmentioning

confidence: 99%

The role of mitochondrial oxidative stress in hearing loss

González-González¹

2017

Neurol Disord Therap

View full text Add to dashboard Cite

Hearing loss is the most common form of sensory impairment in humans, affecting 5.3% worldwide population. Although approximately 1 in 500 children are born with impaired hearing, sudden or progressive forms of hearing loss can manifest at any age. Hearing impairment following cochlear damage due to noise trauma, ototoxicity or age-related cochlear degeneration was linked to a common pathogenesis involving the formation of reactive oxygen species (ROS). This review summarizes the current data suggesting a role of mitochondrial ROS overproduction in hearing loss and the molecular mechanism involved in hair cell apoptosis responsible of this disorder. Because increasing number of studies demonstrated that antioxidants and free radical scavengers may serve as effective compounds to block the activation of cochlear hair cell death, targeting members of antioxidant pathways and in the breakdown of superoxide anions and hydrogen peroxidase, could be feasible options for the treatment of several types of hearing loss.Correspondence to: Sergio Gonzalez-Gonzalez, CILcare, 2214, Boulevard de la Lironde. Parc Scientifique Agropolis, Montpellier, France, E-mail: sergio. gonzalez@cilcare.com Cochlea and hair cellsThe mammalian cochlea is the sensory organ capable of perceiving sound over a range of pressure, and discriminating both infrasonic and ultrasonic frequencies in different species. The organ of Corti is located in the cochlea of the inner ear and is responsible for the detection of sound. This organ harbours the auditory sensory epithelium, which, in humans, contains approximately 16,000 hair cells that are patterned into three rows of outer hair cells (OHCs) and one row of inner hair cells (IHCs) [1,2]. Each hair cell contains, at its apical surface, a mechanically sensitive organelle that consists of rows of actin-filled stereocilia that increasein height. An extracellular matrix, the tectorial membrane, covers the apical surface of the organ of Corti and is attached to the hair bundles of OHCs. The cell bodies of hair cells form specialized adhesive contacts with supporting cells that adhere at their basolateral surfaces to the basilar membrane, an extracellular matrix assembly with a different molecular composition from the tectorial membrane [3,4].Hearing is initiated when sound waves that reach the outer ear travel through the ear canal to the tympanic membrane. Then, the sound energy is transferred, via the bony ossicles of the middle ear, to the oval window at the base of the fluid-filled cochlea. The motions of the oval window are converted into fluid pressure waves that induce vibrations in the basilar membrane. Then, the vibrations are transferred onto the hair cells, leading to the deflection of the hair cell stereocilia [5]. This deflection causes stretch-sensitive ion channels to open. These are non-selectively permeable to cations and are located at the base of the tip links, with 1 or 2 channels per tip link. Stereocilia bathe in endolymph, which is rich in potassium and characterized by an ...

show abstract

Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss

Cited by 153 publications

References 100 publications

Bovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells

Bovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells

Pathophysiology of the cochlear intrastrial fluid-blood barrier (review)

The role of mitochondrial oxidative stress in hearing loss

Contact Info

Product

Resources

About