Proliferation and neuronal differentiation of mitotically active cells following traumatic brain injury

Rice, Ann C.; Khaldi, Ahmad; Harvey, H. B.; Salman, Nadim; White, Frances K.H.; Fillmore, Helen L.; Bullock, M. Ross

doi:10.1016/s0014-4886(03)00241-3

Cited by 175 publications

(124 citation statements)

References 54 publications

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“…The second major finding of this study indicates that nestin is not just upregulated in repopulating and Nestin in the injured glomerulus C Daniel et al proliferating MCs, but also has a function in MC proliferation but not in migration. Earlier studies described nestin as a marker of highly proliferative [36][37][38][39] and migrating cells. 37 In the kidney, a recent study showed nestin-positive cells migrating from the renal papilla to the cortex after ischemia/ reperfusion, 40 indicating a potential role of nestin also for renal cell migration.…”

Section: Nestin In the Injured Glomerulus C Daniel Et Almentioning

confidence: 99%

Nestin expression in repopulating mesangial cells promotes their proliferation

Daniel

Albrecht

Lüdke

et al. 2008

Laboratory Investigation

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We investigated whether the intermediate filament protein and neural stem cell marker nestin characterizes the glomerular progenitor/reserve cell population immigrating the glomerulus after mesangial cell (MC) injury in the rat (antiThy1 nephritis). Nestin expression was investigated by immunohistochemistry and real-time PCR during anti-Thy1 nephritis. Migration and proliferation assays were used to characterize the function of nestin in isolated MCs after nestin knockdown by siRNA. After MC injury during anti-Thy1 nephritis, glomerular nestin was transiently increased during the repopulation phase. At the peak of mesangial proliferation and expansion (day 5) most OX-7-positive MCs expressed nestin largely colocalizing with the activation marker a-smooth muscle actin and the proliferation marker PCNA. In contrast to a healthy, non-injured mesangium in vivo, MCs in culture are considered to be in an 'activated, injured state' and express nestin in a generalized distribution with condensed localization around the nucleus as well as intensive staining of cell protrusions such as filopodia. During cell cycle, the percentage of MCs with high nestin levels was increased during S-and G2-phase. Blocking of nestin using specific siRNA resulted in inhibition of cell proliferation but not cell migration. In conclusion, nestin is constitutively expressed in podocytes, but is a marker for repopulating MCs after experimental MC injury in vivo. Nestin promotes MC proliferation in vitro, suggesting a supporting role for nestin during repair reaction.

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Section: Nestin In the Injured Glomerulus C Daniel Et Almentioning

confidence: 99%

Nestin expression in repopulating mesangial cells promotes their proliferation

Daniel

Albrecht

Lüdke

et al. 2008

Laboratory Investigation

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“…For example, damage induced by mechanical lesions, prolonged seizures, hypoglycemia, fluid percussion injury or stroke increases dentate gyrus cell proliferation by approximately 5-to 12-fold. As in the intact brain, many newly generated cells die, but the vast majority of those that survive differentiate into neurons, and typically less than 20% of adult-born cells become glia or remain undifferentiated (Gould and Tanapat, 1997;Parent et al, 1997;Liu et al, 1998;Jin et al, 2001;Rice et al, 2003;Suh et al, 2005).…”

Section: Influence Of Brain Injury On Adult Neurogenesismentioning

confidence: 99%

“…For example, damage caused by trauma, seizures or focal ischemia accelerates cell proliferation in both the dentate gyrus and SVZ-olfactory bulb pathway of adult rodents (Parent et al, 1997;Liu et al, 1998;Jin et al, 2001;Zhang et al, 2001b;Chirumamilla et al, 2002;Chen et al, 2004;Rice et al, 2003). Precursor progeny give rise mainly to neurons in both regions, although this finding is likely biased in part by the timing of BrdU administration relative to injury; proliferating astrocytes, microglial and endothelial cells also are found (Liu et al, 2001;Parent et al, 2002b).…”

Section: Influence Of Brain Injury On Adult Neurogenesismentioning

confidence: 99%

Adult Neurogenesis and the Ischemic Forebrain

Lichtenwalner

Parent

2005

J Cereb Blood Flow Metab

261

190

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The recent identification of endogenous neural stem cells and persistent neuronal production in the adult brain suggests a previously unrecognized capacity for self-repair after brain injury. Neurogenesis not only continues in discrete regions of the adult mammalian brain, but new evidence also suggests that neural progenitors form new neurons that integrate into existing circuitry after certain forms of brain injury in the adult. Experimental stroke in adult rodents and primates increases neurogenesis in the persistent forebrain subventricular and hippocampal dentate gyrus germinative zones. Of greater relevance for regenerative potential, ischemic insults stimulate endogenous neural progenitors to migrate to areas of damage and form neurons in otherwise dormant forebrain regions, such as the neostriatum and hippocampal pyramidal cell layer, of the mature brain. This review summarizes the current understanding of adult neurogenesis and its regulation in vivo, and describes evidence for stroke-induced neurogenesis and neuronal replacement in the adult. Current strategies used to modify endogenous neurogenesis after ischemic brain injury also will be discussed, as well as future research directions with potential for achieving regeneration after stroke and other brain insults.

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“…Although the functional significance is still not clear, accumulating evidence has indicated that neurogenesis may play an important role in the maintenance of normal hippocampal functions such as learning and memory (van Praag, et al, 2000, Shors, et al, 2001, Aimone, et al, 2006 and may be modulated by environmental factors (Kempermann, et al, 1997, Rampon, et al, 2000, van Praag, et al, 2000, stress (Mirescu andGould, 2006, Warner-Schmidt andDuman, 2006) and antidepressants (Santarelli, et al, 2003, Duman, 2004. Moreover, certain acute brain injuries such as ischemia, hypoxia, seizures, and trauma increase neurogenesis (Kokaia and Lindvall, 2003, Rice, et al, 2003, Itoh, et al, 2005, Overstreet-Wadiche, et al, 2006, Qiu, et al, 2007, suggesting that neurogenesis may work as a protective mechanism for the brain. Interestingly, enhanced neurogenesis was recently found in brains of neurodegenerative diseases including Huntington's disease (Curtis, et al, 2003), Parkinson's disease (Hoglinger, et al, 2004), and AD (Jin, et al, 2004a).…”

Section: Introductionmentioning

confidence: 99%

Adult neurogenesis is functionally associated with AD-like neurodegeneration

Chen

Nakajima

Choi

et al. 2008

Neurobiology of Disease

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Alzheimer's disease (AD) is predominantly characterized by progressive neuronal loss in the brain. It has been recently found that adult neurogenesis in the hippocampal dentate gyrus of AD patients is significantly enhanced, while its functional significance is still unknown. By using an AD-like neurodegeneration mouse model, we show here that neurogenesis in the dentate gyrus was neurodegenerative stage-dependent. At early stages of neurodegeneration, neurogenesis was significantly enhanced and newly generated neurons migrated into the local neuronal network. Up to late stages of neurodegeneration, however, the survival of newly generated neurons was impaired so that the enhanced neurogenesis could not be detected any more. Most interestingly, these dynamic changes in neurogenesis were correlated with the severity of neuronal loss in the dentate gyrus, indicating that neurogenesis may work as a self-repairing mechanism to compensate for neurodegeneration. Therefore, to enhance endogenous neurogenesis at early stages of neurodegeneration may be a valuable strategy to delay neurodegenerative progress.

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Proliferation and neuronal differentiation of mitotically active cells following traumatic brain injury

Cited by 175 publications

References 54 publications

Nestin expression in repopulating mesangial cells promotes their proliferation

Nestin expression in repopulating mesangial cells promotes their proliferation

Adult Neurogenesis and the Ischemic Forebrain

Adult neurogenesis is functionally associated with AD-like neurodegeneration

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