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Book ; Online: Aging, neurogenesis and neuroinflammation in hearing loss and protection

Milo, Marta / Varela-Nieto, Isabel / Magarinos, Marta

2015

Abstract: Worldwide, 278 million people are estimated to have moderate to profound hearing loss. Age-related hearing loss, also known as presbyacusis, affects approximately half of the population over 60 years old, making it the second most common cause of ... ...

Abstract	Worldwide, 278 million people are estimated to have moderate to profound hearing loss. Age-related hearing loss, also known as presbyacusis, affects approximately half of the population over 60 years old, making it the second most common cause of disability in older people. Hearing loss occurs when the sensory cells and neurons of the cochlea degenerate and die. The vestibular system, which holds the sense of balance, shares a common embryonic origin with the cochlea and together conform the inner ear. Balance problems are a trait of ageing to the point that balance ability is considered a sensor of physical decline and vestibular degeneration is the most common cause of falls in the elderly. Still the molecular bases of ageing in the vestibular system have not been studied in detail. Genetic and environmental factors contribute to the progression of age-related hearing loss (ARHL). Being noise the main environmental noxious agent for human hearing in the industrialized societies. There is no restorative treatment for deafness but functional replacement by means of prosthesis. Therefore, prevention and treatment of hearing loss is an unmet medical need. To develop innovative medical strategies against hearing loss, it is critical to understand the causes of ARHL and the essential pathways responsible for the manifestation of this complex disease. In this research topic, experts will discuss the stages and molecular elements of the damage and repair processes involved in ARHL, from cellular processes to molecules involved in aging. Oxidative stress takes a central stage as an essential element in the progression of injury and cell loss, and a target for cell protection strategies. Finally, the mechanisms of action and the potential of novel therapies for hair cell repair and protection will be discussed along with drug delivery strategies
Keywords	Science (General) ; Neurosciences. Biological psychiatry. Neuropsychiatry
Size	1 electronic resource (151 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020091834
ISBN	9782889196449 ; 2889196445
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article: Ceramide Kinase Inhibition Blocks IGF-1-Mediated Survival of Otic Neurosensory Progenitors by Impairing AKT Phosphorylation.

León, Yolanda / Magariños, Marta / Varela-Nieto, Isabel

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 678760

Abstract: Sphingolipids are bioactive lipid components of cell membranes with important signal transduction functions in health and disease. Ceramide is the central building block for sphingolipid biosynthesis and is processed to form structurally and functionally ...

Abstract	Sphingolipids are bioactive lipid components of cell membranes with important signal transduction functions in health and disease. Ceramide is the central building block for sphingolipid biosynthesis and is processed to form structurally and functionally distinct sphingolipids. Ceramide can be phosphorylated by ceramide kinase (CERK) to generate ceramide-1-phosphate, a cytoprotective signaling molecule that has been widely studied in multiple tissues and organs, including the developing otocyst. However, little is known about ceramide kinase regulation during inner ear development. Using chicken otocysts, we show that genes for CERK and other enzymes of ceramide metabolism are expressed during the early stages of inner ear development and that
Language	English
Publishing date	2021-06-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.678760
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Article ; Online: Complementary and distinct roles of autophagy, apoptosis and senescence during early inner ear development.

Varela-Nieto, Isabel / Palmero, Ignacio / Magariños, Marta

Hearing research

2019 Volume 376, Page(s) 86–96

Abstract: The development of the inner ear complex cytoarchitecture and functional geometry requires the exquisite coordination of a variety of cellular processes in a temporal manner. At early stages of inner ear development several rounds of cell proliferation ... ...

Abstract	The development of the inner ear complex cytoarchitecture and functional geometry requires the exquisite coordination of a variety of cellular processes in a temporal manner. At early stages of inner ear development several rounds of cell proliferation in the otocyst promote the growth of the structure. The apoptotic program is initiated in exceeding cells to adjust cell type numbers. Apoptotic cells are cleared by phagocytic cells that recognize the phosphatidylserine residues exposed in the cell membrane thanks to the energy supplied by autophagy. Specific molecular programs determine hair and supporting cell fate, these populations are responsible for the functions of the adult sensory organ: detection of sound, position and acceleration. The neurons that transmit auditory and balance information to the brain are also born at the otocyst by neurogenesis facilitated by autophagy. Cellular senescence participates in tissue repair, cancer and aging, situations in which cells enter a permanent cell cycle arrest and acquire a highly secretory phenotype that modulates their microenvironment. More recently, senescence has also been proposed to take place during vertebrate development in a limited number of transitory structures and organs; among the later, the endolymphatic duct in the inner ear. Here, we review these cellular processes during the early development of the inner ear, focusing on how the most recently described cellular senescence participates and cooperates with proliferation, apoptosis and autophagy to achieve otic morphogenesis and differentiation.
MeSH term(s)	Animals ; Apoptosis/physiology ; Autophagy/physiology ; Cell Differentiation/physiology ; Cell Proliferation/physiology ; Cellular Senescence/physiology ; Ear, Inner/cytology ; Ear, Inner/embryology ; Ear, Inner/physiology ; Humans ; Mice ; Models, Biological ; Morphogenesis/physiology
Language	English
Publishing date	2019-01-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	282629-x
ISSN	1878-5891 ; 0378-5955
ISSN (online)	1878-5891
ISSN	0378-5955
DOI	10.1016/j.heares.2019.01.014
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dysfunction of programmed embryo senescence is linked to genetic developmental defects.

de Lope, Cristina / García-Lucena, Rebeca / Magariños, Marta / León, Yolanda / Casa-Rodríguez, Nuria / Contreras, Nuria / Escudero-Iriarte, Carmen / Varela-Nieto, Isabel / Maire, Pascal / Palmero, Ignacio

Development (Cambridge, England)

2023 Volume 150, Issue 9

Abstract: Developmental senescence is a form of programmed senescence that contributes to morphogenesis during embryonic development. We showed recently that the SIX1 homeoprotein, an essential regulator of organogenesis, is also a repressor of adult cellular ... ...

Abstract	Developmental senescence is a form of programmed senescence that contributes to morphogenesis during embryonic development. We showed recently that the SIX1 homeoprotein, an essential regulator of organogenesis, is also a repressor of adult cellular senescence. Alterations in the SIX/EYA pathway are linked to the human branchio-oto-renal (BOR) syndrome, a rare congenital disorder associated with defects in the ears, kidneys and branchial arches. Here, we have used Six1-deficient mice, an animal model of the BOR syndrome, to investigate whether dysfunction of senescence underpins the developmental defects associated with SIX1 deficiency. We have focused on the developing inner ear, an organ with physiological developmental senescence that is severely affected in Six1-deficient mice and BOR patients. We show aberrant levels and distribution of senescence markers in Six1-deficient inner ears concomitant with defective morphogenesis of senescent structures. Transcriptomic analysis and ex vivo assays support a link between aberrant senescence and altered morphogenesis in this model, associated with deregulation of the TGFβ/BMP pathway. Our results show that misregulation of embryo senescence may lead to genetic developmental disorders, significantly expanding the connection between senescence and disease.
MeSH term(s)	Adult ; Humans ; Mice ; Animals ; Protein Tyrosine Phosphatases/physiology ; Intracellular Signaling Peptides and Proteins/metabolism ; Nuclear Proteins/genetics ; Ear, Inner ; Branchio-Oto-Renal Syndrome/genetics ; Homeodomain Proteins/metabolism
Chemical Substances	Protein Tyrosine Phosphatases (EC 3.1.3.48) ; Intracellular Signaling Peptides and Proteins ; Nuclear Proteins ; Homeodomain Proteins ; SIX1 protein, human
Language	English
Publishing date	2023-05-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.200903
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Zs.MG 91: Show issues

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Article: Otic Neurogenesis Is Regulated by TGFβ in a Senescence-Independent Manner.

Magariños, Marta / Barajas-Azpeleta, Raquel / Varela-Nieto, Isabel / R Aburto, Maria

Frontiers in cellular neuroscience

2020 Volume 14, Page(s) 217

Abstract: Cellular senescence has classically been associated with aging. Intriguingly, recent studies have also unraveled key roles for senescence in embryonic development, regeneration, and reprogramming. Developmental senescence has been reported during ... ...

Abstract	Cellular senescence has classically been associated with aging. Intriguingly, recent studies have also unraveled key roles for senescence in embryonic development, regeneration, and reprogramming. Developmental senescence has been reported during embryonic development in different organisms and structures, such as the endolymphatic duct during inner ear development of mammals and birds. However, there is no study addressing the possible role of senescence on otic neurogenesis. TGFβ/SMAD is the best-known pathway linked to the induction of developmentally programmed cell senescence. Here, we studied if TGFβ2 induces cellular senescence during acoustic-vestibular-ganglion (AVG) formation. Using organotypic cultures of AVG, and characterizing different stages of otic neurogenesis in the presence of TGFβ2 and a selective TGF-β receptor type-I inhibitor, we show that TGFβ2 exerts a powerful action in inner ear neurogenesis but, contrary to what we recently observed during endolymphatic duct development, these actions are independent of cellular senescence. We show that TGFβ2 reduces proliferation, and induces differentiation and neuritogenesis of neuroblasts, without altering cell death. Our studies highlight the roles of TGFβ2 and cellular senescence in the precise regulation of cell fate within the developing inner ear and its different cell types, being their mechanisms of action highly cell-type dependent.
Language	English
Publishing date	2020-08-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2020.00217
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Article: Editorial: Aging, neurogenesis and neuroinflammation in hearing loss and protection.

Magariños, Marta / Milo, Marta / Varela-Nieto, Isabel

Frontiers in aging neuroscience

2015 Volume 7, Page(s) 138

Language	English
Publishing date	2015-07-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2015.00138
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TGFβ2-induced senescence during early inner ear development.

Gibaja, Alejandro / Aburto, María R / Pulido, Sara / Collado, Manuel / Hurle, Juan M / Varela-Nieto, Isabel / Magariños, Marta

Scientific reports

2019 Volume 9, Issue 1, Page(s) 5912

Abstract: Embryonic development requires the coordinated regulation of apoptosis, survival, autophagy, proliferation and differentiation programs. Senescence has recently joined the cellular processes required to master development, in addition to its well- ... ...

Abstract	Embryonic development requires the coordinated regulation of apoptosis, survival, autophagy, proliferation and differentiation programs. Senescence has recently joined the cellular processes required to master development, in addition to its well-described roles in cancer and ageing. Here, we show that senescent cells are present in a highly regulated temporal pattern in the developing vertebrate inner ear, first, surrounding the otic pore and, later, in the otocyst at the endolymphatic duct. Cellular senescence is associated with areas of increased apoptosis and reduced proliferation consistent with the induction of the process when the endolymphatic duct is being formed. Modulation of senescence disrupts otic vesicle morphology. Transforming growth factor beta (TGFβ) signaling interacts with signaling pathways elicited by insulin-like growth factor type 1 (IGF-1) to jointly coordinate cellular dynamics required for morphogenesis and differentiation. Taken together, these results show that senescence is a natural occurring process essential for early inner ear development.
MeSH term(s)	Animals ; Cell Differentiation ; Cellular Senescence ; Chickens ; Ear, Inner/growth & development ; Ear, Inner/metabolism ; Embryo, Mammalian/cytology ; Embryo, Mammalian/metabolism ; Gene Expression Regulation, Developmental ; Mice ; Organogenesis ; Signal Transduction ; Transforming Growth Factor beta2/genetics ; Transforming Growth Factor beta2/metabolism
Chemical Substances	Tgfb2 protein, mouse ; Transforming Growth Factor beta2
Language	English
Publishing date	2019-04-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-42040-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Autophagy in the Vertebrate Inner Ear.

Magariños, Marta / Pulido, Sara / Aburto, María R / de Iriarte Rodríguez, Rocío / Varela-Nieto, Isabel

Frontiers in cell and developmental biology

2017 Volume 5, Page(s) 56

Abstract: Autophagy is a conserved catabolic process that results in the lysosomal degradation of cell components. During development, autophagy is associated with tissue and organ remodeling, and under physiological conditions it is tightly regulated as it plays ... ...

Abstract	Autophagy is a conserved catabolic process that results in the lysosomal degradation of cell components. During development, autophagy is associated with tissue and organ remodeling, and under physiological conditions it is tightly regulated as it plays a housekeeping role in removing misfolded proteins and damaged organelles. The vertebrate inner ear is a complex sensory organ responsible for the perception of sound and for balance. Cell survival, death and proliferation, as well as cell fate specification and differentiation, are processes that are strictly coordinated during the development of the inner ear in order to generate the more than a dozen specialized cell types that constitute this structure. Here, we review the existing evidence that implicates autophagy in the generation of the vertebrate inner ear. At early stages of chicken otic development, inhibiting autophagy impairs neurogenesis and causes aberrant otocyst morphogenesis. Autophagy provides energy for the clearing of dying cells and it favors neuronal differentiation. Moreover, autophagy is required for proper vestibular development in the mouse inner ear. The autophagy-related genes
Language	English
Publishing date	2017-05-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2017.00056
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Article ; Online: C-Raf deficiency leads to hearing loss and increased noise susceptibility.

de Iriarte Rodríguez, Rocío / Magariños, Marta / Pfeiffer, Verena / Rapp, Ulf R / Varela-Nieto, Isabel

Cellular and molecular life sciences : CMLS

2015 Volume 72, Issue 20, Page(s) 3983–3998

Abstract: The family of RAF kinases transduces extracellular information to the nucleus, and their activation is crucial for cellular regulation on many levels, ranging from embryonic development to carcinogenesis. B-RAF and C-RAF modulate neurogenesis and ... ...

Abstract	The family of RAF kinases transduces extracellular information to the nucleus, and their activation is crucial for cellular regulation on many levels, ranging from embryonic development to carcinogenesis. B-RAF and C-RAF modulate neurogenesis and neuritogenesis during chicken inner ear development. C-RAF deficiency in humans is associated with deafness in the rare genetic insulin-like growth factor 1 (IGF-1), Noonan and Leopard syndromes. In this study, we show that RAF kinases are expressed in the developing inner ear and in adult mouse cochlea. A homozygous C-Raf deletion in mice caused profound deafness with no evident cellular aberrations except for a remarkable reduction of the K(+) channel Kir4.1 expression, a trait that suffices as a cause of deafness. To explore the role of C-Raf in cellular protection and repair, heterozygous C-Raf (+/-) mice were exposed to noise. A reduced C-RAF level negatively affected hearing preservation in response to noise through mechanisms involving the activation of JNK and an exacerbated apoptotic response. Taken together, these results strongly support a role for C-RAF in hearing protection.
MeSH term(s)	Animals ; Apoptosis/genetics ; Cochlea/metabolism ; Ear, Inner/embryology ; Ear, Inner/metabolism ; Female ; Hearing Loss/genetics ; Hearing Loss/metabolism ; Male ; Mice ; Noise ; Proto-Oncogene Proteins c-raf/genetics ; Proto-Oncogene Proteins c-raf/metabolism ; Proto-Oncogene Proteins c-raf/physiology ; Signal Transduction
Chemical Substances	Proto-Oncogene Proteins c-raf (EC 2.7.11.1)
Language	English
Publishing date	2015-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-015-1919-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Autophagy during vertebrate development.

Aburto, María R / Hurlé, Juan M / Varela-Nieto, Isabel / Magariños, Marta

Cells

2012 Volume 1, Issue 3, Page(s) 428–448

Abstract: Autophagy is an evolutionarily conserved catabolic process by which cells degrade their own components through the lysosomal machinery. In physiological conditions, the mechanism is tightly regulated and contributes to maintain a balance between ... ...

Abstract	Autophagy is an evolutionarily conserved catabolic process by which cells degrade their own components through the lysosomal machinery. In physiological conditions, the mechanism is tightly regulated and contributes to maintain a balance between synthesis and degradation in cells undergoing intense metabolic activities. Autophagy is associated with major tissue remodeling processes occurring through the embryonic, fetal and early postnatal periods of vertebrates. Here we survey current information implicating autophagy in cellular death, proliferation or differentiation in developing vertebrates. In developing systems, activation of the autophagic machinery could promote different outcomes depending on the cellular context. Autophagy is thus an extraordinary tool for the developing organs and tissues.
Language	English
Publishing date	2012-08-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells1030428
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