Biology Stack Exchange is a question and answer site for biology researchers, academics, and students. Join them; it only takes a minute:

Sign up
Here's how it works:
  1. Anybody can ask a question
  2. Anybody can answer
  3. The best answers are voted up and rise to the top

I am studying a case of tendinopathies induced by an alteration of how the extracellular matrix is being remodeled.

From my understanding there has to be a careful balance of MMP (metallproteinases) and TIMP enzymes to maintain tendon homeostasis.

Which cells produce these enzymes?

share|improve this question
up vote 3 down vote accepted

Taken from The role of matrix metalloproteinases (MMPs) in the pathophysiology of chronic obstructive pulmonary disease

Metalloelastase (MMP-12) is (as the name suggests) capable of degrading elastin, as well as other extra-cellular matrix components. It is produced predominantly by infiltrating macrophages and appears essential for macrophage migration through extra-cellular matrix

Matrix Metalloproteinases in Cancer Cell Invasion gives a more thorough description of the various MMP and TIMP types

MMPs are mainly produced by nonmalignant stromal cells in malignant tumors. Tumor cells also secrete factors, such as extracellular MMP inducer (EMMPRIN), which enhance the expression of MMPs by stromal fibroblasts (see Toole, in this book). In addition, growth factors and cytokines secreted by tumor-infiltrating inflammatory cells as well as by tumor or stromal cells modulate MMP expression.

share|improve this answer
Thanks for your input... I am trying to understand how Fluoroquinolone drugs can degrade tendons. From what I am understand MMP-9 is of my concern: "Our study provides preliminary evidence that topical application of fluoroquinolone drugs can induce the expression of MMP-1, MMP-2, MMP-8 and MMP-9 in the undebrided corneal epithelium compared to artificial tear eye drops." ( – user952 Jun 6 '12 at 20:53
Here's another one: Ciprofloxacin enhances the stimulation of matrix metalloproteinase 3 expression by interleukin-1beta in human tendon-derived cells. A potential mechanism of fluoroquinolone-induced tendinopathy. – Noam Kremen Jun 8 '12 at 8:33

Your Answer


By posting your answer, you agree to the privacy policy and terms of service.

Not the answer you're looking for? Browse other questions tagged or ask your own question.