instruction:
In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
question:
Context: The present study was designed to investigate whether H2S can protect testicular germ cells against heat exposure induced injury and the underlying mechanisms.', 'It was found that all three H2S generating enzymes, cystathionine β-synthase (CBS), cystathionine γ-lysase (CSE), and 3-mercaptopyruvate sulfurtransferase (3 MST), were expressed in mouse testicular tissue. Three episodes of heat exposure (42 °C, 30 min/day, 3 days) significantly decreased endogenous H2S production and down-regulated the expression of CBS and CSE in testes. In primary cultured testicular germ cells, exogenous application of NaHS (an H2S donor) attenuated heat stress (42 °C, 30 min) induced cell death and apoptosis. This was mediated by the inhibitory effects of H2S on cytochrome C release and the ratio of the Bax/Bcl-2. NaHS also improved mitochondrial function by decreasing oxygen consumption and increasing ATP production. NaHS treatment also stimulated SOD activity and reduced ROS production.\Question: Does hydrogen sulfide protect testicular germ cells against heat-induced injury?
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Our results revealed both physiological and pharmacological roles of H2S in testicular germ cells. Exogenous application of H2S may protect germ cells by preservation of mitochondrial function and stimulation of anti-oxidant activity.


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Context: Proliferation of smooth muscle cells (SMCs) plays an important role in vascular pathobiology, being involved in the development of coronary restenosis and atherosclerosis. The activation of nuclear proto-oncogenes appears to be a final common pathway onto which various mitogenic signals coverage. Accordingly, we attempted to determine whether the activation of the c-myc nuclear proto-oncogene is essential for human SMC proliferation and explored the possibility of inhibiting their growth using antisense oligonucleotides directed against c-myc messenger RNA (mRNA).', 'Proliferation of human SMCs was associated with an increase in c-myc mRNA expression after growth stimulation. Using 15-mer phosphorothioate oligonucleotides (oligomers), we tested their growth-inhibitory effect in SMCs in vitro. Antisense oligomers directed against the translation initiation region of the human c-myc gene exhibited a significant antiproliferative effect, whereas sense and mismatched oligomers did not inhibit the growth. The growth-inhibitory effect of c-myc antisense oligomers was dose dependent and preventable by an excess of sense oligomers. Furthermore, growth inhibition of SMCs treated with c-myc antisense oligomers was associated with a marked decrease in the c-myc mRNA level. Phosphorothioate oligomers remained stable in medium containing 20% serum and were detectable in SMCs as early as 1 hour after cell exposure. Intact oligomers rapidly accumulated intracellularly and persisted within human SMCs for at least 16 hours.\Question: Does downregulation of c-myc expression by antisense oligonucleotides inhibit proliferation of human smooth muscle cells?
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c-myc antisense oligomers reduced c-myc expression and produced a significant growth inhibition of human SMCs, indicating an important role of c-myc gene activation in the process of SMC proliferation. Furthermore, extracellular stability and rapid cellular uptake provide the basis for future studies assessing the therapeutic role of the c-myc antisense approach in reducing SMC proliferation in the process of vascular restenosis.


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Context: Coxsackie and adenovirus receptor is a high affinity receptor for adenovirus type 5. To our knowledge the expression profile of coxsackie and adenovirus receptor in renal cancer has not been described. We evaluated the expression of coxsackie and adenovirus receptor in human renal cancer specimens and determined whether the histone deacetylase inhibitor FK-228 (Astelas Pharmaceutical, Osaka, Japan) increases the efficiency of adenoviral infections in renal carcinoma cells in vivo and in vitro.', 'We used randomly selected renal cancer specimens. Specimens were analyzed for coxsackie and adenovirus receptor expression using reverse transcriptase-polymerase chain reaction and immunohistochemistry. In vitro experiments on cytotoxicity were performed to determine a nontoxic dose of FK-228 for renal cancer cells. The level of coxsackie and adenovirus receptor expression was determined by fluorescence activated cell scanning and/or reverse transcriptase-polymerase chain reaction in FK-228 treated renal cancer cells. The effect in vivo on adenoviral gene expression was investigated in athymic mice.', 'In several human renal cancer specimens a loss of or decreased coxsackie and adenovirus receptor expression was detected by reverse transcriptase-polymerase chain reaction based analysis and immunohistochemistry. The nontoxic dose of FK-228 for renal carcinoma cells was 0.5 ng/ml. Treatment of cancer cells with 0.5 ng/ml FK-228 increased levels of coxsackie and adenovirus receptor RNA and acetylated histone H3. This increase was associated with an approximately 10-fold increase in adenoviral infection, as evidenced by increased transgene expression from a beta-galactosidase containing adenoviral vector. Intravenous administration of FK-228 enhanced coxsackie and adenovirus receptor expression in athymic mice. The combination of beta-galactosidase adenovirus and FK-228 was significantly more effective than adenovirus only in A498 cells 3 weeks after treatment in vivo. The combination of p21 adenovirus and FK-228 resulted in significant tumor inhibition in vitro and in vivo.\Question: Does a histone deacetylase inhibitor enhance adenoviral infection of renal cancer cells?
answer:

In human renal cancer specimens a loss of or decrease in coxsackie and adenovirus receptor expression may be an early event in renal cancer progression. Pretreatment with FK-228 may increase tumor cell sensitivity to adenoviral gene therapy vectors.