Harrod K S, Olson J W, Gillespie M N
Division of Pharmacology and Experimental Therapeutics, College of Pharmacy, University of Kentucky, A.B. Chandler Medical Center, Lexington 40536-0082, USA.
Am J Physiol. 1996 Jul;271(1 Pt 1):L31-7. doi: 10.1152/ajplung.1996.271.1.L31.
The polyamines are a family of low-molecular-weight organic cations that play essential intracellular regulatory roles in cell growth and differentiation. Elevations in cellular polyamine contents necessary for most physiological and pathological events in the lung appear to be driven by increase de novo synthesis. In contrast, increases in lung cell polyamines required for hypoxic pulmonary vascular disease can be attributed to augmented transmembrane polyamine transport which may, in turn, be the result of hypoxia-related decreases in the activity of the initial and generally rate-limiting enzyme in de novo polyamine synthesis, ornithine decarboxylase (ODC). To begin to define the unusual mechanism whereby hypoxia governs polyamine regulatory pathways, the present study examined the impact of varying severity and durations of hypoxic exposure on ODC activity and mRNA content in cultured bovine main pulmonary artery smooth muscle cells (PASMC). The effect of hypoxia on the activity of another rate-limiting enzyme in polyamine synthesis, S-adenosylmethionine decarboxylase (AdoMet-DC), also was examined. Hypoxia caused time-dependent decreases in ODC and AdoMet-DC activities that were related to the severity of hypoxic exposure. Similarly, ODC mRNA content also was depressed by hypoxic exposure. The relationship between the decline in ODC activity and mRNA content was roughly linear. To determine whether hypoxia impairs ODC mRNA stability, two different inhibitors of transcription and Northern analyses were used to follow the decay in ODC mRNA abundance in hypoxic and normoxic PASMC. Densitometric scanning of Northern analysis indicated that ODC mRNA stability did not differ between hypoxic and normoxic PASMC. These results suggest that the reduction in ODC activity provoked by hypoxia in cultured bovine PASMC can be ascribed in part to a diminished transcriptional rate rather than to alterations in mRNA stability.
多胺是一类低分子量有机阳离子,在细胞生长和分化过程中发挥着重要的细胞内调节作用。肺中大多数生理和病理事件所必需的细胞内多胺含量升高似乎是由从头合成增加所驱动的。相比之下,低氧性肺血管疾病所需的肺细胞多胺增加可归因于跨膜多胺转运增强,而这反过来可能是由于从头多胺合成中初始且通常为限速酶鸟氨酸脱羧酶(ODC)活性因缺氧而降低的结果。为了开始明确缺氧调控多胺调节途径的异常机制,本研究检测了不同严重程度和持续时间的缺氧暴露对培养的牛主肺动脉平滑肌细胞(PASMC)中ODC活性和mRNA含量的影响。还检测了缺氧对多胺合成中另一种限速酶S-腺苷甲硫氨酸脱羧酶(AdoMet-DC)活性的影响。缺氧导致ODC和AdoMet-DC活性随时间下降,这与缺氧暴露的严重程度相关。同样,缺氧暴露也降低了ODC mRNA含量。ODC活性下降与mRNA含量之间的关系大致呈线性。为了确定缺氧是否损害ODC mRNA稳定性,使用了两种不同的转录抑制剂和Northern分析来追踪缺氧和常氧PASMC中ODC mRNA丰度的衰减。Northern分析的光密度扫描表明,缺氧和常氧PASMC之间ODC mRNA稳定性没有差异。这些结果表明,培养的牛PASMC中缺氧引起的ODC活性降低部分可归因于转录速率降低,而非mRNA稳定性改变。