Post-stroke gaseous hypothermia increases vascular density but not neurogenesis in the ischemic penumbra of aged rats
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Post-stroke gaseous hypothermia increases vascular density but not neurogenesis in the ischemic penumbra of aged rats. / Sandu, Raluca Elena; Uzoni, Adriana; Ciobanu, Ovidiu; Moldovan, Mihai; Anghel, Andrei; Radu, Eugen; Coogan, Andrew N.; Popa-Wagner, Aurel.
In: Restorative Neurology and Neuroscience, Vol. 34, No. 3, 2016, p. 401-414.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Post-stroke gaseous hypothermia increases vascular density but not neurogenesis in the ischemic penumbra of aged rats
AU - Sandu, Raluca Elena
AU - Uzoni, Adriana
AU - Ciobanu, Ovidiu
AU - Moldovan, Mihai
AU - Anghel, Andrei
AU - Radu, Eugen
AU - Coogan, Andrew N.
AU - Popa-Wagner, Aurel
PY - 2016
Y1 - 2016
N2 - Purpose: In aged humans, stroke is a major cause of disability for which no neuroprotective measures are available. In animal studies of focal ischemia, short-term hypothermia often reduces infarct size. Nevertheless, efficient neuroprotection requires long-term, regulated lowering of whole body temperature. Previously, we reported that post-stroke exposure to hydrogen sulfide (H2S) effectively lowers whole body temperature and confers neuroprotection in aged animals. Methods: In the present study using behavioral tests, MRI, telemetrical EEG, BP and temperature recordings, RT-PCR and immunofluorescence, we assessed infarct size, vascular density, neurogenesis and as well as the expression of genes coding for proteasomal proteins as well as in post-stroke aged Sprague-Dawley rats exposed to H2S- induced hypothermia. Results: Two days exposure to mild hypothermia diminishes the expression of several genes involved in protein degradation, thereby leading to better preservation of infarcted tissue. Further, hypothermia increased the density of newly formed blood vessels in the peri-lesional cortex did not enhance neurogenesis in the infarcted area of aged rats. Likewise, there was improved recovery of fine vestibulomotor function and asymmetric sensorimotor deficit. Conclusion: Long-term hypothermia may be a viable clinical approach by simultaneously targeting multiple processes including better tissue preservation, enhanced vascular density and improved behavioral performance.
AB - Purpose: In aged humans, stroke is a major cause of disability for which no neuroprotective measures are available. In animal studies of focal ischemia, short-term hypothermia often reduces infarct size. Nevertheless, efficient neuroprotection requires long-term, regulated lowering of whole body temperature. Previously, we reported that post-stroke exposure to hydrogen sulfide (H2S) effectively lowers whole body temperature and confers neuroprotection in aged animals. Methods: In the present study using behavioral tests, MRI, telemetrical EEG, BP and temperature recordings, RT-PCR and immunofluorescence, we assessed infarct size, vascular density, neurogenesis and as well as the expression of genes coding for proteasomal proteins as well as in post-stroke aged Sprague-Dawley rats exposed to H2S- induced hypothermia. Results: Two days exposure to mild hypothermia diminishes the expression of several genes involved in protein degradation, thereby leading to better preservation of infarcted tissue. Further, hypothermia increased the density of newly formed blood vessels in the peri-lesional cortex did not enhance neurogenesis in the infarcted area of aged rats. Likewise, there was improved recovery of fine vestibulomotor function and asymmetric sensorimotor deficit. Conclusion: Long-term hypothermia may be a viable clinical approach by simultaneously targeting multiple processes including better tissue preservation, enhanced vascular density and improved behavioral performance.
KW - Aging
KW - HS
KW - hypothermia
KW - neurogenesis
KW - proteasome
KW - stroke
KW - vascular density
U2 - 10.3233/RNN-150600
DO - 10.3233/RNN-150600
M3 - Journal article
C2 - 26923618
AN - SCOPUS:84975492973
VL - 34
SP - 401
EP - 414
JO - Restorative Neurology and Neuroscience
JF - Restorative Neurology and Neuroscience
SN - 0922-6028
IS - 3
ER -
ID: 179282288