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Effects of aging on neural stem/progenitor cells and oligodendrocyte precursor cells after focal cerebral ischemia in spontaneously hypertensive rats

机译：衰老对自发性高血压大鼠局灶性脑缺血后神经干/祖细胞和少突胶质前体细胞的影响

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Aging and vascular comorbidities such as hypertension comprise critical co-factors that influence how the brain responds to stroke. Ischemic stress induces neurogenesis and oligodendrogenesis in younger brains. However, it remains unclear whether these compensatory mechanisms can be maintained even under pathologic hypertensive and aged states. To clarify the age-related remodeling capacity after stroke under hypertensive conditions, we assessed infarct volume, behavioral outcomes, and surrogate markers of neurogenesis and oligodendrogenesis in acute and sub-acute phases after transient focal cerebral ischemia in 3 month old and 12 month old spontaneously hypertensive rats (SHRs). Hematoxylin and eosin staining showed that 3 and 12 month old SHRs exhibited similar infarction volumes at both 3 and 14 days after focal cerebral ischemia. However, recovery of behavioral deficits (neurological score assessment and adhesive removal test) were significantly less in 12-month-old SHRs compared to 3-month-old SHRs. Concomitantly, numbers of nestin-positive neural stem/progenitor cells (NSPCs) near the infarct border area or subventricular zone in 12-moth-old SHRs were lower than 3-month-old SHRs at day 3. Similarly, numbers of PDGF-R-α-positive oligodendrocyte precursor cells (OPCs) in corpus callosum was lower in 12-month-old SHRs at day 3. Lower levels of NSPC and OPC numbers were accompanied by lower expression levels of CREB phosphorylation. By day 14 post-ischemia, NSPC and OPC numbers in 12-month-old SHRs recovered to similar levels as in 3-month-old SHRs. But the numbers of proliferating NSPCs (Ki67+nestin+ cells) and proliferating OPCs (Ki67+PDGF-R-α+ cells) remained lower in the older brains even at day 14. Taken together, these findings suggest that aging may also decrease post-stroke compensatory responses for neurogenesis and oligodendrogenesis even under hypertensive conditions.
机译：诸如高血压之类的衰老和血管合并症是影响大脑对中风反应方式的关键辅助因素。缺血性应激会在年轻的大脑中诱导神经发生和少突胶质生成。然而，尚不清楚即使在病理性高血压和老年状态下，这些补偿机制是否也能维持。为了阐明高血压条件下中风后与年龄相关的重塑能力，我们评估了3个月大和12个月大的短暂性局灶性脑缺血后急性和亚急性期的梗死体积，行为结局以及神经发生和少突胶质形成的替代标志物高血压大鼠（SHRs）。苏木精和曙红染色显示3个月和12个月大的SHR在局灶性脑缺血后3和14天表现出相似的梗塞体积。然而，与3个月大的SHR相比，12个月大的SHR的行为缺陷恢复（神经学评分评估和粘胶去除测试）明显更少。同时，在第3天，在12个月大的SHR中，梗塞边界区域或脑室下区域附近的巢蛋白阳性神经干/祖细胞（NSPC）的数量低于3个月大的SHR。在第3天，call体中的-α阳性少突胶质前体细胞（OPCs）在12个月大的SHR中较低。NSPC和OPC含量较低时，CREB磷酸化表达水平较低。缺血后第14天，12个月大的SHR中的NSPC和OPC数量恢复到与3个月大的SHR中相似的水平。但是增殖的NSPC（Ki67 + nestin + 细胞）和增殖的OPC（Ki67 + PDGF-R-α + <甚至在第14天，较老的大脑中的细胞）仍保持较低水平。综上所述，这些发现表明，即使在高血压条件下，衰老也可能减少中风后对神经发生和少突胶质形成的代偿反应。

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