Lee A Baldridge

Publications (2)7.85 Total impact

• Article: Ectopic prostatic tissue: histogenesis and histopathological characteristics.

  Shams Halat, John N Eble, David J Grignon, Shannon Lacy, Rodolfo Montironi, Gregory T MacLennan, Antonio Lopez-Beltran, Puay-Hoon Tan, Lee A Baldridge, Liang Cheng
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  ABSTRACT: To evaluate the histological and immunohistochemical characteristics of ectopic prostatic tissue. We studied 20 cases of ectopic prostate. In 85% (17/20) of the cases, the ectopic prostatic tissue was located in the bladder; in the remaining cases, it was located in the urethra. In 60% of the cases (12/20), no significant inflammatory or reactive/reparative changes were identified in the adjacent tissue. Immunohistochemical stains for prostate-specific antigen, prostate-specific acid phosphatase, and prostein were positive in the glandular epithelial cells of all cases. Stains for 34βE12 and p63 confirmed the presence of basal cells in all cases. There was no overexpression of α-methylacyl-CoA racemase in any of the cases. There was cytoplasmic luminal staining for CD10 and cytoplasmic staining for cytokeratin 18 in acinar cells in all cases. In cases in which followup data were available, no patient was found to have residual or recurrent ectopic prostatic tissue and none developed prostatic adenocarcinoma. Ectopic prostatic tissue is occasionally encountered in the lower urinary tract, most commonly in the bladder and urethra of males. Ectopic prostatic tissue has histological and immunohistochemical characteristics that are indistinguishable from those of normal prostatic tissue, and most likely represents the persistence of embryonic structures.
  Histopathology 03/2011; 58(5):750-8. · 3.08 Impact Factor
• Article: Mechanical stimulation of bone in vivo reduces osteocyte expression of Sost/sclerostin.

  Alexander G Robling, Paul J Niziolek, Lee A Baldridge, Keith W Condon, Matthew R Allen, Imranul Alam, Sara M Mantila, Jelica Gluhak-Heinrich, Teresita M Bellido, Stephen E Harris, Charles H Turner
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  ABSTRACT: Sclerostin, the protein product of the Sost gene, is a potent inhibitor of bone formation. Among bone cells, sclerostin is found nearly exclusively in the osteocytes, the cell type that historically has been implicated in sensing and initiating mechanical signaling. The recent discovery of the antagonistic effects of sclerostin on Lrp5 receptor signaling, a crucial mediator of skeletal mechanotransduction, provides a potential mechanism for the osteocytes to control mechanotransduction, by adjusting their sclerostin (Wnt inhibitory) signal output to modulate Wnt signaling in the effector cell population. We investigated the mechanoregulation of Sost and sclerostin under enhanced (ulnar loading) and reduced (hindlimb unloading) loading conditions. Sost transcripts and sclerostin protein levels were dramatically reduced by ulnar loading. Portions of the ulnar cortex receiving a greater strain stimulus were associated with a greater reduction in Sost staining intensity and sclerostin-positive osteocytes (revealed via in situ hybridization and immunohistochemistry, respectively) than were lower strain portions of the tissue. Hindlimb unloading yielded a significant increase in Sost expression in the tibia. Modulation of sclerostin levels appears to be a finely tuned mechanism by which osteocytes coordinate regional and local osteogenesis in response to increased mechanical stimulation, perhaps via releasing the local inhibition of Wnt/Lrp5 signaling.
  Journal of Biological Chemistry 03/2008; 283(9):5866-75. · 4.77 Impact Factor