Biomedical subjects

C Yan

Publications and source records attributed to C Yan.

At least 55 records · Page 3Linked to original sources

PubMed2001

Stage and cell-specific expression of calmodulin-dependent phosphodiesterases in mouse testis.

Calcium and cyclic nucleotides are second messengers that regulate the development and functional activity of spermatozoa. Calcium/calmodulin-dependent phosphodiesterases (CaM-PDEs) are abundant in testicular cells and in mature spermatozoa and provide one means by which calcium regulates cellular cyclic nucleotide content. We examined the spatial and temporal expression profiles of three knownCaM-PDE genes, PDE1A, PDE1B, and PDE1C, in the testis. In situ hybridization and immunofluorescent staining showed that both PDE1A and PDE1C are highly expressed but at different stages in developing germ cells. However, a very low hybridization signal of PDE1B exists uniformly throughout the seminiferous epithelium and the interstitium. More specifically, PDE1A mRNA is found in round to elongated spermatids, with protein expression in the tails of elongated and maturing spermatids. In contrast, PDE1C mRNA accumulates during early meiotic prophase and throughout meiotic and postmeiotic stages. Immunocytochemistry showed a diffuse, presumably cytosolic distribution of the expressed protein. The distinct spatial and temporal expression patterns of CaM-PDEs suggest important but different physiological roles for these CaM-PDEs in developing and mature spermatozoa.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2001

Intracellular Bax translocation after transient cerebral ischemia: implications for a role of the mitochondrial apoptotic signaling pathway in ischemic neuronal death.

Activation of terminal caspases such as caspase-3 plays an important role in the execution of neuronal cell death after transient cerebral ischemia. Although the precise mechanism by which terminal caspases are activated in ischemic neurons remains elusive, recent studies have postulated that the mitochondrial cell death-signaling pathway may participate in this process. The bcl-2 family member protein Bax is a potent proapoptotic molecule that, on translocation from cytosol to mitochondria, triggers the activation of terminal caspases by increasing mitochondrial membrane permeability and resulting in the release of apoptosis-promoting factors, including cytochrome c. In the present study, the role of intracellular Bax translocation in ischemic brain injury was investigated in a rat model of transient focal ischemia (30 minutes) and reperfusion (1 to 72 hours). Immunochemical studies revealed that transient ischemia induced a rapid translocation of Bax from cytosol to mitochondria in caudate neurons, with a temporal profile and regional distribution coinciding with the mitochondrial release of cytochrome c and caspase-9. Further, in postischemic caudate putamen in vivo and in isolated brain mitochondria in vitro, the authors found enhanced heterodimerization between Bax and the mitochondrial membrane permeabilization-related proteins adenine nucleotide translocator (ANT) and voltage-dependent anion channel. The ANT inhibitor bongkrekic acid prevented Bax and ANT interactions and inhibited Bax-triggered caspase-9 release from isolated brain mitochondria in vitro. Bongkrekic acid also offered significant neuroprotection against ischemia-induced caspase-3 and caspase-9 activation and cell death in the brain. These results strongly suggest that the Bax-mediated mitochondrial apoptotic signaling pathway may play an important role in ischemic neuronal injury.

Animals↗

PubMed2001

Endothelial atheroprotective and anti-inflammatory mechanisms.

Atherosclerosis preferentially occurs in areas of turbulent flow and low fluid shear stress, whereas laminar flow and high shear stress are atheroprotective. Inflammatory cytokines, such as tumor necrosis factor-alpha (TNF), have been shown to stimulate expression of endothelial cell (EC) genes that may promote atherosclerosis. Recent data suggest that steady laminar flow decreases EC apoptosis and blocks TNF-mediated EC activation. EC apoptosis is likely important in the process termed "plaque erosion" that leads to platelet aggregation. Steady laminar flow inhibits EC apoptosis by preventing cell cycle entry, by increasing antioxidant mechanisms (e.g., superoxide dismutase), and by stimulating nitric oxide-dependent protective pathways that involve enzymes PI3-kinase and Akt. Conversely, our laboratory has identified nitric oxide-independent mechanisms that limit TNF signal transduction. TNF regulates gene expression in EC, in part, by stimulating mitogen-activated protein kinases (MAPK) which phosphorylate transcription factors. We hypothesized that fluid shear stress modulates TNF effects on EC by inhibiting TNF-mediated activation of MAP kinases. To test this hypothesis, we determined the effects of steady laminar flow (shear stress = 12 dynes/cm2) on TNF-stimulated activity of two MAP kinases: extracellular signal regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK). Flow alone stimulated ERK1/2 activity, but decreased JNK activity compared to static controls. TNF (10 ng/ml) alone activated both ERK1/2 and JNK maximally at 15 minutes in human umbilical vein EC (HUVEC). Pre-exposing HUVEC for 10 minutes to flow inhibited TNF activation of JNK by 46%, but it had no significant effect on ERK1/2 activation. Incubation of EC with PD98059, a specific mitogen-activated protein kinase kinase inhibitor, blocked the flow-mediated inhibition of TNF activation of JNK. Flow-mediated inhibition of JNK was unaffected by 0.1 mM L-nitroarginine, 100 pM 8-bromo-cyclic GMP, or 100 microM 8-bromo-cyclic AMP. Transfection studies with dominant negative constructs of the protein kinase MEK1 and MEK5 suggested an important role for BMK1 in flow-mediated regulation of TNF signals. In summary, the atheroprotective effects of steady laminar flow on the endothelium involve multiple synergistic mechanisms.

Animals↗

PubMed2001

Analysis of ovarian gene expression in follicle-stimulating hormone beta knockout mice.

FSH is a heterodimeric glycoprotein hormone that is produced in the gonadotroph cells of the anterior pituitary. It acts on Sertoli cells of the testis and granulosa cells of the ovary. We previously demonstrated that FSHbeta knockout female mice are infertile due to a block in folliculogenesis preceding antral stage development. To investigate aberrations of ovarian gene regulation in the absence of FSH, we analyzed the expression of several important marker genes using Northern blot and in situ hybridization techniques. Key findings are as follows: 1) Follicles of FSHbeta knockout mice develop a well organized thecal layer, which is positive for P450 17alpha-hydroxylase and LH receptor messenger RNAs (mRNAs). This indicates that theca recruitment is completed autonomously with respect to FSH. 2) Granulosa cells in FSH-deficient mice demonstrate an increase in FSH receptor mRNA, and decreases in P450 aromatase, serum/glucocorticoid-induced kinase, and inhibin/activin subunit mRNAs. These data support studies that implicate FSH signaling cascades in the expression of these genes. 3) In contrast to the thecal layer, granulosa cell populations in FSHbeta knockout mice do not accumulate LH receptor mRNA. This suggests that although the granulosa cells have a block in proliferation at the antral follicle stage in the absence of FSH, they do not initiate programs of terminal differentiation as seen in luteinizing cells of wild-type ovaries. 4) Ovaries of FSH-deficient mice demonstrate a modest decrease in cyclin D2 mRNA, without up-regulation of cell cycle inhibitor mRNAs associated with luteinization (i.e. p15, p27, and p21). Although components of the FSH null phenotype may be caused by partial cyclin D2 loss of function, these findings indicate that the mechanisms of granulosa cell cycle arrest in FSHbeta knockout mice are distinct from those of cycle withdrawal at luteinization. Underscoring the usefulness of the FSH-deficient mouse model, this study clarifies aspects of gonadotropin-dependent folliculogenesis, thecal layer development, cycle control in granulosa cells, and luteinization.

Animals↗

PubMed2001

Synergistic roles of bone morphogenetic protein 15 and growth differentiation factor 9 in ovarian function.

Knockout mouse technology has been used over the last decade to define the essential roles of ovarian-expressed genes and uncover genetic interactions. In particular, we have used this technology to study the function of multiple members of the transforming growth factor-beta superfamily including inhibins, activins, and growth differentiation factor 9 (GDF-9 or Gdf9). Knockout mice lacking GDF-9 are infertile due to a block in folliculogenesis at the primary follicle stage. In addition, recombinant GDF-9 regulates multiple cumulus granulosa cell functions in the periovulatory period including hyaluronic acid synthesis and cumulus expansion. We have also cloned an oocyte-specific homolog of GDF-9 from mice and humans, which is termed bone morphogenetic protein 15 (BMP-15 or Bmp15). To define the function of BMP-15 in mice, we generated embryonic stem cells and knockout mice, which have a null mutation in this X-linked gene. Male chimeric and Bmp15 null mice are normal and fertile. In contrast to Bmp15 null males and Gdf9 knockout females, Bmp15 null females (Bmp15(-/-)) are subfertile and usually have minimal ovarian histopathological defects, but demonstrate decreased ovulation and fertilization rates. To further decipher possible direct or indirect genetic interactions between GDF-9 and BMP-15, we have generated double mutant mice lacking one or both alleles of these related homologs. Double homozygote females (Bmp15(-/-)Gdf9(-/-)) display oocyte loss and cysts and resemble Gdf9(-/-) mutants. In contrast, Bmp15(-/-)Gdf9(+/-) female mice have more severe fertility defects than Bmp15(-/-) females, which appear to be due to abnormalities in ovarian folliculogenesis, cumulus cell physiology, and fertilization. Thus, the dosage of intact Bmp15 and Gdf9 alleles directly influences the destiny of the oocyte during folliculogenesis and in the periovulatory period. These studies have important implications for human fertility control and the maintenance of fertility and normal ovarian physiology.

Animals↗

PubMed2001

[Expression of tumor suppressor genes p16, p21 and p53 in a pair of lung adenocarcinoma cell lines with different metastasis potentials: Anip973 and AGZY83-a].

OBJECTIVE: In order to investigate the suppression effect of tumor suppressor genes in lung adenocarcinoma. METHODS: p16 and p21 expression vectors were transfected into a pair of lung adenocarcinoma cell lines with different metastasis potentials: Anip973(high metastasis potential)and AGZY83-a (low metastasis potential). In the mean time, AGZY83-a, Anip973, AGZY83-ap16 and Anip973p16 were infected with recombinant adenovirus encoding wild- type p53 gene. The suppression effects of these genes were evaluated by cell growth curve, MTT, cloning efficiency assay, flow cytometric analysis and TUNEL technique. RESULTS: Overexpression of p16 gene in Anip973 and AGZY83-a could only lengthen the G(1) phase while increased expression of p21 in both of the cell lines was associated with significant lengthening of G(1) phase, decreased proliferation potential and decreased cloning efficiency. High efficient expression of wild-type p53 gene in AGZY83-a, Anip973, Anip973p16 and AGZY83-ap16 inhibited the growth of these four kinds of lung cancer cells and killed the cells in the end. Apoptosis was detected in all the four kinds of cells. The suppression effect of p53 gene was higher in Anip973 and Anip973p16 than in AGZY83-a and AGZY83-ap16 while co-expression of p53 and p16 in this pair of cell lines inhibited the cells more efficiently as compared with the expression of p53 gene. CONCLUSION: Increased expression of p21 gene suppressed the lung adenocarcinoma cells by G(1) arrest and the co-transfection of tumor suppressor genes p16 and p53 into the lung adenocarcinoma cell line proved more effective in lung cancer gene therapy.

Adenocarcinoma↗

PubMed2001

Analysis of 20 mature ovarian cystic teratoma cases in postmenopausal women.

OBJECTIVE: To study the incidence of malignant change, diagnosis and management of mature cystic teratomas in postmenopausal women. METHODS: Twenty cases of mature cystic teratoma in postmenopausal women admitted to our hospital between January 1977 and January 1997 was retrospectively reviewed and evaluated. RESULTS: The number of postmenopausal patients with mature cystic teratoma (20) accounted for 7.6% of the total number of patients with benign ovarian teratomas (263). There were 3 cases of malignant change, which were squamous carcinoma, carcinosarcoma, and digestive gland epithelial carcinoma. The incidence of malignant change was 15%. CONCLUSION: In postmenopausal women, mature ovarian cystic teratoma should be treated as lowly malignant and should be paid much attention.

Combined Modality Therapy↗

PubMed2001

Relationship between HLA-DRB1 and DQ alleles and the genetic susceptibility to type 1 diabetes.

OBJECTIVE: To study the relationship between human leukocyte antigen (HLA)-DRB1 and DQ alleles and the genetic susceptibility of type 1 diabetes in North Chinese children. METHODS: Polymerase chain reaction (PCR) techniques were used to amplify the second exon of DRB1 and DQ alleles, after which sequence specific olignucleotide probe (SSOP) dot blot hybridization techniques were used to analyze the amplified products. RESULTS: DRB1 * 0301, DQA1 * 0301, DQB1 * 0201 alleles and DRB1 * 0301-DQA1 * 0501-DQB1 * 0201 haplotype were significantly increased in patients, while DQA1 * 0103 and DQB1 * 0601 alleles were significantly increased in controls. The distribution of DR4 and DR9 haplotypes in patients and controls were not significantly different, but DR3/DR4 and DR4/DR9 heterozygotes were significantly increased in patients. CONCLUSIONS: DRB1 * 0301, DQA1 * 0301 and DQB1 * 0201 confer susceptibility while DQA1 * 0103 and DQB1 * 0601 confer protection to type 1 diabetes. DRB1 * 0301-DQA1 * 0501-DQB1 * 0201 haplotype offers a predisposition to type 1 diabetes in North Chinese. Although the distribution of DR4 and DR9 in patients and controls had no significant difference, DR3/DR4 and DR3/DR9 heterozygotes were significantly increased in patients, showing that the susceptive effects of DR3 and DR4 or DR4 and DR9 haplotypes could be added up.

Alleles↗

PubMed2001

[Enantiomeric separations of 1-1,2,4-triazole compounds by micro-high performance liquid chromatography].

The enantiomeric separations of sixteen novel 1-1,2,4-triazole chiral compounds were investigated by micro-HPLC with a 200 mm x 100 microns i.d. capillary chiral OD column. The detection was performed at 223 nm. The mobile phase was a mixture of iso-propyl alcohol and n-hexane(20:80, V/V) at a flow rate of 30 microL/min and column head pressure of 6.9 MPa. Some of the enantiomers could be separated on baseline. In comparing with the separation results by the conventional HPLC method, the micro-HPLC method had the advantages of high-speed, economy, environmental friendliness etc. The effect of solute structure on enantio-selectivity was investigated and the chiral recognition mechanism was also discussed. It was found that the main separation mechanisms involve the pi-pi association and inclusion between the substituent R and the spiral pocket of OD-CSP.

2-Propanol↗

PubMed2001

[Rapid synthesis and fluorescent spectra of the phosphor CaS:Eu2+ in a microwave field].

In this paper, the phosphors with CaS as the host and doped with Eu2+ ion were synthesized in a microwave field at the first time. The influence of the different concentrations of Eu2+ ion on fluorescent properties of the phosphors CaS:Eu2+ was discussed. The experimental results of SEM show that the crystallite structures of the CaS:Eu2+ with different shapes (such as cubic, spherical and rod) and different crystal sizes (100-1,500 nm), for example, nano-scale, submicron-scale or micron-scale can be obtained when doping different concentrations of Eu2+ ion. The fluorescent intensity of the sphere phosphor CaS:Eu2+ is the strongest under the excitation at 254 nm.

Calcium Sulfate↗

PubMed2000

Cyclophilin A is a secreted growth factor induced by oxidative stress.

Reactive oxygen species have been implicated in the pathogenesis of atherosclerosis, hypertension, and restenosis, in part by promoting vascular smooth muscle cell (VSMC) growth. Many VSMC growth factors are secreted by VSMC and act in an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member of the immunophilin family, is secreted by VSMCs in response to oxidative stress and mediates extracellular signal-regulated kinase (ERK1/2) activation and VSMC growth by reactive oxygen species. Human recombinant CyPA can mimic the effects of secreted CyPA to stimulate ERK1/2 and cell growth. The peptidyl-prolyl isomerase activity is required for ERK1/2 activation by CyPA. In vivo, CyPA expression and secretion are increased by oxidative stress and vascular injury. These findings are the first to identify CyPA as a secreted redox-sensitive mediator, establish CyPA as a VSMC growth factor, and suggest an important role for CyPA and enzymes with peptidyl-prolyl isomerase activity in the pathogenesis of vascular diseases.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

PubMed2000

Pressurized gradient capillary electrochromatographic separation of eighteen amino acid derivatives.

A pressurized gradient capillary electrochromatography (pCEC) instrument was developed to separate 18 amino acid derivatives. A reversed-phase C18 column (3 microm, 130 mm x 75 microm I.D.) and an acetate buffer (50 mmol/l NaAc, pH 6.4) with an ion-pair reagent (1% N,N-dimethylformamide) were used to separate derivatized amino acids from a standard solution (2 microg/ml), and the wavelength of the UV-Vis detector was 360 nm. The pressure on the capillary column was kept at approx. 70 Pa and 3 kV positive voltage was added on the outlet end of column. The effect of voltage on the eluting order of amino acids and the resolution of separation were studied, and it was found that when the voltage was higher than 3 kV, the adsorption of amino acids in the porous C18 column occurred. The effect of salt concentration, injection volume, and column length on the separation of amino acids was determined. The amino acid sample was separated by pCEC, and RSDs of the migration times of each amino acid were all less than 2.5%.

Amino Acids↗

PubMed2000

Growth differentiation factor-9 stimulates progesterone synthesis in granulosa cells via a prostaglandin E2/EP2 receptor pathway.

Growth differentiation factor-9 (GDF-9), an oocyte-secreted member of the transforming growth factor beta superfamily, progesterone receptor, cyclooxygenase 2 (Cox2; Ptgs2), and the EP2 prostaglandin E(2) (PGE(2)) receptor (EP2; Ptgerep2) are required for fertility in female but not male mice. To define the interrelationship of these factors, we used a preovulatory granulosa cell culture system in which we added recombinant GDF-9, prostaglandins, prostaglandin receptor agonists, or cyclooxygenase inhibitors. GDF-9 stimulated Cox2 mRNA within 2 h, and PGE(2) within 6 h; however, progesterone was not increased until 12 h after addition of GDF-9. This suggested that Cox2 is a direct downstream target of GDF-9 but that progesterone synthesis required an intermediate. To determine whether prostaglandin synthesis was required for progesterone production, we analyzed the effects of PGE(2) and cyclooxygenase inhibitors on this process. PGE(2) can stimulate progesterone synthesis by itself, although less effectively than GDF-9 (3-fold vs. 6-fold increase over 24 h, respectively). Furthermore, indomethacin or NS-398, inhibitors of Cox2, block basal and GDF-9-stimulated progesterone synthesis. However, addition of PGE(2) to cultures containing both GDF-9 and NS-398 overrides the NS-398 block in progesterone synthesis. To further define the PGE(2)-dependent pathway, we show that butaprost, a specific EP2 agonist, stimulates progesterone synthesis and overrides the NS-398 block. In addition, GDF-9 stimulates EP2 mRNA synthesis by a prostaglandin- and progesterone-independent pathway. Thus, GDF-9 induces an EP2 signal transduction pathway which appears to be required for progesterone synthesis in cumulus granulosa cells. These studies further demonstrate the importance of oocyte-somatic cell interactions in female reproduction.

Alprostadil↗

PubMed2000

Fullerene-sensitized

[reaction: see text] Fullerene catalyzes the cycloaddition of dimethyliminodiacetate to maleimides under photolysis to form 2,5-dimethoxycarbonylpyrrolidine derivatives.

Journal Article↗

PubMed2000

Oocyte-expressed TGF-beta superfamily members in female fertility.

Folliculogenesis is regulated by the interplay of extraovarian and intraovarian factors, and the importance of each type of regulation varies depending on the developmental stage of the follicle. Preantral follicle development is regulated predominantly by factors produced locally within the ovary and within the follicle itself. The oocyte has been shown to produce soluble factor(s), which regulate a number of processes in follicular development, including cumulus expansion in the periovulatory period. Members of the TGFbeta superfamily are potent regulators of cell proliferation and differentiation in a number of organ systems, and three members, growth differentiation factor 9 (GDF-9), bone morphogenetic protein 15 (BMP-15) and BMP-6 are expressed by the oocyte and may mediate effects attributed to the oocyte. Based on knockout mouse models BMP-6 does not play an essential role in ovarian function, but GDF-9 is absolutely required for preantral follicle development. GDF-9 also alters the periovulatory expression of granulosa cell genes and stimulates cumulus expansion. Although BMP-15 is expressed identically to GDF-9, its role in regulating ovarian function is still unknown. This review examines the similarities and differences in sequence, expression, and function of the oocyte-expressed TGFbeta family members with respect to regulating folliculogenesis.

Animals↗

PubMed2000

Retinoic acid stimulation of the human surfactant protein B promoter is thyroid transcription factor 1 site-dependent.

Surfactant B (SP-B) is a 79-amino acid peptide critical to postnatal respiratory adaptation. Expression of SP-B by respiratory epithelial cells is regulated by developmental and hormonal influences at the level of gene transcription. Previous studies supported the role of retinoic acids (RA) and their receptors (RARs) in SP-B gene transcription. In the present study, RARalpha was detected in mouse alveolar type II epithelial cells where SP-B is synthesized and processed. Deletion and site-specific mutagenesis analysis identified clustered retinoic acid-responsive element sites in the 5'-flanking enhancer region of the hSP-B gene that bound RARalpha proteins. RAR coactivators ACTR, SRC-1, and transcriptional intermediary factor 2 (TIF2) stimulated human (h) SP-B promoter activity in a dose-dependent fashion in pulmonary adenocarcinoma H441 cells. In addition, an RAR-associated protein, CREB-binding protein (CBP), potentiated the effects of RAR on hSP-B promoter activity in H441 cells. Importantly, RA stimulation of the hSP-B promoter depends on tissue-specific thyroid transcription factor (TTF-1) DNA-binding sites. TTF-1 protein synergistically stimulated the hSP-B promoter with RARalpha, CBP, and nuclear receptor coactivators in H441 cells. In addition, TTF-1 interacted directly with RARalpha and TIF2 in the mammalian two-hybrid system. These findings support a model in which RAR/retinoid X receptor, TTF-1, coactivators, and CBP form a transcription activation complex in the upstream enhancer region of the hSP-B gene.

Animals↗

PubMed2000

Separation of related opiate compounds using capillary electrochromatography.

Capillary electrophoretic separations have been investigated for six controlled narcotic analgesic compounds having related structures. Owing to the similar charge-to-mass ratios of these compounds, capillary zone electrophoresis failed to provide a satisfactory separation, whereas a baseline-resolved separation was achieved in 10 min using micellar electrokinetic chromatography. Column efficiencies of 40,000-150,000 plates/m were obtained with a 50 cm long, 50 microm inner diameter (ID) capillary using 50 mM sodium dodecyl sulfate (SDS) in a 50 mM borate solution containing 12% isopropanol. In contrast, separation of this mixture by capillary electrochromatography proved to be significantly superior. The capillary was 15 cm long, with an ID of 75 microm, and was packed with 1.5 microm nonporous octadecyl silica (ODS) particles. The mobile phase consisted of 80% 10 mM tris(hydroxymethyl)aminomethane (Tris) and 20% acetonitrile, and contained 5 mM SDS. A complete separation was obtained in 2.5 min with an efficiency of 250,000-500,000 plates/m.

Analgesics, Opioid↗

PubMed2000

Overexpression of the cell death suppressor Bcl-w in ischemic brain: implications for a neuroprotective role via the mitochondrial pathway.

Bcl-w is a newly described cell death suppressor member of the Bcl-2 gene family. As these genes may have a role in the outcome of ischemic brain injury, the regional expression of Bcl-w protein in rat brain was examined at 6 to 72 hours after 90 minutes of transient middle cerebral artery occlusion. Bcl-w protein, although constitutively expressed at low levels in nonischemic brain, was found to be overexpressed in ischemic brain at all time points studied. Up-regulation of Bcl-w protein was particularly abundant in the penumbral region of the cortex and mainly in cells lacking DNA fragmentation. In the cortical penumbra, Bcl-w protein was detected predominantly in neurons and showed mitochondrial localization, as determined using double-label immunohistochemistry. Bcl-w expression was also detectable, to a lesser extent, in reactive astrocytes in the infarct border zone and in microvessel walls in the infarct regions. At the mechanistic level, incubation of isolated brain mitochondria with the addition of recombinant Bax or high concentration of calcium resulted in release of cytochrome c from the mitochondria. In the presence of recombinant Bcl-w protein, however, the release of cytochrome c induced by Bax or calcium was largely inhibited. Further, recombinant Bcl-w protein inhibited calcium-induced loss of mitochondrial transmembrane potential, indicative of permeability transition, in a dose-dependent manner. These results suggest that Bcl-w may be an endogenous neuroprotectant against ischemic neuronal death and that, like its analogues such as Bcl-2 and Bcl-x-long, Bcl-w may achieve this protection via the mitochondrial death-regulatory pathway.

Animals↗